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0 ] "en" => array:8 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">COMMENTS</span>" "titulo" => "First Brazilian pediatric hospital to adopt 1-hour preoperative fasting time for clear fluids for elective surgeries" "tienePdf" => "en" "tieneTextoCompleto" => "en" "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Priscilla Ferreira Neto Cardoso, Vinicius Caldeira Quintão, Bruno Perini, Maria José Carvalho Carmona, Ricardo Vieira Carlos, Cláudia Marquez Simões" "autores" => array:6 [ 0 => array:2 [ "nombre" => "Priscilla Ferreira Neto" "apellidos" => "Cardoso" ] 1 => array:2 [ "nombre" => "Vinicius Caldeira" "apellidos" => "Quintão" ] 2 => array:2 [ "nombre" => "Bruno" "apellidos" => "Perini" ] 3 => array:2 [ "nombre" => "Maria José Carvalho" "apellidos" => "Carmona" ] 4 => array:2 [ "nombre" => "Ricardo Vieira" "apellidos" => "Carlos" ] 5 => array:2 [ "nombre" => "Cláudia Marquez" "apellidos" => "Simões" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S1807593222002484?idApp=UINPBA00004N" "url" => "/18075932/000000760000000C/v1_202211191031/S1807593222002484/v1_202211191031/en/main.assets" ] "itemAnterior" => array:19 [ "pii" => "S1807593222002460" "issn" => "18075932" "doi" => "10.6061/clinics/2021/e3312" "estado" => "S300" "fechaPublicacion" => "2021-01-01" "aid" => "246" "copyright" => "CLINICS" "documento" => "article" "crossmark" => 0 "licencia" => "https://creativecommons.org/licenses/by/4.0/" "subdocumento" => "fla" "cita" => "Clinics. 2021;76C:" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:11 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">ORIGINAL ARTICLE</span>" "titulo" => "Relationship of the Pelvic-Trochanteric Index with greater trochanteric pain syndrome" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => "en" "contieneResumen" => array:1 [ "en" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig3" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 945 "Ancho" => 1300 "Tamanyo" => 88510 ] ] "descripcion" => array:1 [ "en" => "<p id="spara30" class="elsevierStyleSimplePara elsevierViewall">Dispersion graphic: age <span class="elsevierStyleItalic">versus</span> pelvic-trochanteric index.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Leandro Emílio Nascimento Santos, Túlio Pinho Navarro, Carla Jorge Machado, Henrique Antônio Berwanger de Amorim Cabrita, Robinson Esteves Pires, Leonardo Brandão Figueiredo, Henrique Melo Campos Gurgel, Rudolf Moreira Pfeilsticker, Helvécio Grandinetti, Amanda Damasceno de Souza, Marco Antônio Percope de Andrade" "autores" => array:11 [ 0 => array:2 [ "nombre" => "Leandro Emílio Nascimento" "apellidos" => "Santos" ] 1 => array:2 [ "nombre" => "Túlio Pinho" "apellidos" => "Navarro" ] 2 => array:2 [ "nombre" => "Carla Jorge" "apellidos" => "Machado" ] 3 => array:2 [ "nombre" => "Henrique Antônio Berwanger de Amorim" "apellidos" => "Cabrita" ] 4 => array:2 [ "nombre" => "Robinson Esteves" "apellidos" => "Pires" ] 5 => array:2 [ "nombre" => "Leonardo Brandão" "apellidos" => "Figueiredo" ] 6 => array:2 [ "nombre" => "Henrique Melo Campos" "apellidos" => "Gurgel" ] 7 => array:2 [ "nombre" => "Rudolf Moreira" "apellidos" => "Pfeilsticker" ] 8 => array:2 [ "nombre" => "Helvécio" "apellidos" => "Grandinetti" ] 9 => array:2 [ "nombre" => "Amanda Damasceno de" "apellidos" => "Souza" ] 10 => array:2 [ "nombre" => "Marco Antônio Percope de" "apellidos" => "Andrade" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S1807593222002460?idApp=UINPBA00004N" "url" => "/18075932/000000760000000C/v1_202211191031/S1807593222002460/v1_202211191031/en/main.assets" ] "en" => array:19 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">ORIGINAL ARTICLE</span>" "titulo" => "RNA-binding protein with serine-rich domain 1 regulates microsatellite instability of uterine corpus endometrial adenocarcinoma" "tieneTextoCompleto" => true "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Xiaojuan Liu, Hui Ma, Lisha Ma, Kun Li, Yanhua Kang" "autores" => array:5 [ 0 => array:2 [ "nombre" => "Xiaojuan" "apellidos" => "Liu" ] 1 => array:2 [ "nombre" => "Hui" "apellidos" => "Ma" ] 2 => array:2 [ "nombre" => "Lisha" "apellidos" => "Ma" ] 3 => array:2 [ "nombre" => "Kun" "apellidos" => "Li" ] 4 => array:4 [ "nombre" => "Yanhua" "apellidos" => "Kang" "email" => array:1 [ 0 => "yanhkang@126.com" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "*" "identificador" => "cor1" ] ] ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "Department of Gynecology and Obstetrics, The First Affiliated Hospital of Hebei North University, Qiaoxi District, Zhangjiakou City 075000, Hebei Province, P.R. China" "identificador" => "aff1" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor1" "etiqueta" => "*" "correspondencia" => "Corresponding author." ] ] ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig2" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 765 "Ancho" => 1754 "Tamanyo" => 181096 ] ] "descripcion" => array:1 [ "en" => "<p id="spara20" class="elsevierStyleSimplePara elsevierViewall">(A) <span class="elsevierStyleItalic">RNPS1</span> expression, (B) quantitation of the <span class="elsevierStyleItalic">RNPS1</span> expression levels from the western blots, and (C) IHC staining analysis for <span class="elsevierStyleItalic">RNPS1</span> in para-tumor and tumor tissues (×400). (D) <span class="elsevierStyleItalic">RNPS1</span> expression in NEC, KLE, RL952, Ishikawa, and ECC-1 cells. (E) Quantitation of the <span class="elsevierStyleItalic">RNPS1</span> expression levels in cells. Protein levels were normalized to those of β-actin. (n=6, *<span class="elsevierStyleItalic">p</span><0.05: tumor <span class="elsevierStyleItalic">vs.</span> para-tumor or RL952 <span class="elsevierStyleItalic">vs.</span> other cells).</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="cesec10" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle60">INTRODUCTION</span><p id="para10" class="elsevierStylePara elsevierViewall">Uterine corpus endometrial carcinoma (UCEC) is a common gynecological carcinoma with a high recurrence rate (<a class="elsevierStyleCrossRef" href="#bib1">1</a>). Endometrioid adenocarcinoma (EC) is the most common pathological manifestation of UCEC, with proliferative endometrial tumor cells showing glandular complexity and cellular pleomorphism (<a class="elsevierStyleCrossRef" href="#bib2">2</a>). The risk of recurrence is intermediate or high in patients with EC after radical hysterectomy combined with pelvic and para-aortic lymphadenectomy, a considerable challenge for clinics (<a class="elsevierStyleCrossRef" href="#bib3">3</a>). Although evolving medical technologies have led to long-term declines in mortality due to EC, the mechanisms and treatment of EC require further exploration.</p><p id="para20" class="elsevierStylePara elsevierViewall">DNA mismatch repair (MMR) protein deficiency is a result of microsatellite instability (MSI), a hallmark of EC (<a class="elsevierStyleCrossRef" href="#bib4">4</a>,<a class="elsevierStyleCrossRef" href="#bib5">5</a>), providing the biological relevance and potential utility of the modal classification of EC and increasing the complexity of the genomic instability underlying tumorigenesis (<a class="elsevierStyleCrossRef" href="#bib6">6</a>). As MMR regulation may be a prognostic factor for patients with advanced UCEC (<a class="elsevierStyleCrossRef" href="#bib7">7</a>,<a class="elsevierStyleCrossRef" href="#bib8">8</a>), an MMR regulator for treating UCEC needs to be identified.</p><p id="para30" class="elsevierStylePara elsevierViewall">RNA-binding protein with serine-rich domain 1 (<span class="elsevierStyleItalic">RNPS1</span>) belongs to the mRNA nuclear export and mRNA surveillance post-splicing multiprotein complex (<a class="elsevierStyleCrossRef" href="#bib9">9</a>) involved in lung squamous cell and ovarian adenocarcinoma (<a class="elsevierStyleCrossRef" href="#bib10">10</a>,<a class="elsevierStyleCrossRef" href="#bib11">11</a>). However, the mechanisms underlying the role of <span class="elsevierStyleItalic">RNPS1</span> in MMR in UCEC remain unclear.</p><p id="para40" class="elsevierStylePara elsevierViewall">The Notch signaling pathway is implicated in many cancers, including in the maintenance of cancer stem cells, metabolism, survival, drug resistance, epithelial-mesenchymal transition, and genomic instability (<a class="elsevierStyleCrossRef" href="#bib12">12</a>). The Notch signaling pathway may enhance the invasive properties of EC, indicating that it may serve as a promising target for the treatment of this malignancy (<a class="elsevierStyleCrossRef" href="#bib13">13</a>).</p><p id="para50" class="elsevierStylePara elsevierViewall">The present study aimed to determine the role of <span class="elsevierStyleItalic">RNPS1</span> in UCEC. We used an <span class="elsevierStyleItalic">RNPS1</span> knockdown lentivirus (sh-RNPS1) to regulate MMR progression through the Notch signaling pathway and tumor progression in UCEC. The present findings indicate that <span class="elsevierStyleItalic">RNPS1</span> regulates MMR in UCEC. These results may provide novel strategies for UCEC therapy <span class="elsevierStyleItalic">via</span> MMR-associated mechanisms.</p></span><span id="cesec20" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle70">MATERIALS AND METHODS</span><span id="cesec30" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle80">UCEC specimens from patients</span><p id="para60" class="elsevierStylePara elsevierViewall">Sixteen patients pathologically diagnosed with moderately differentiated (G2), type I, MMR-deficient EC were selected at the Department of Pathology of the First Affiliated Hospital of Hebei North University from May 2019 to May 2021, with adjacent para-carcinoma tissues serving as controls. All patients provided written informed consent to participate and the use of their samples was approved by the ethics committee of this study.</p></span><span id="cesec40" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle90">Bioinformatics analysis</span><p id="para70" class="elsevierStylePara elsevierViewall">The expression of <span class="elsevierStyleItalic">RNPS1</span> in various types of cancers was analyzed using TIMER2.0 (<a href="http://http://timer.cistrome.org/">http://timer.cistrome.org/</a>). Gene set enrichment analysis (GSEA) data were analyzed as previously described (<a class="elsevierStyleCrossRef" href="#bib14">14</a>). The survival of patients with UCEC showing low and high <span class="elsevierStyleItalic">RNPS1</span> expression was assayed using the Kaplan-Meier plotter (<a href="http://http://kmplot.com/analysis/">http://kmplot.com/analysis/</a>). Pan-cancer was analyzed as previously described (<a class="elsevierStyleCrossRef" href="#bib15">15</a>). Genes related to mutation and prognosis were analyzed using target gene assays (<a href="https://www.mutarget.com/analysis?type=target">https://www.mutarget.com/analysis?type=target</a>).</p></span><span id="cesec50" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle100">Cell lines and cell culture</span><p id="para80" class="elsevierStylePara elsevierViewall">Normal endometrial (NECs; CP-H058), KLE (CL-0133), RL952 (CL-0197), and Ishikawa (CL-0283) cells (all from Procell, Wuhan, China) and ECC-1 cells (BS-C163325, BinSuiBio, Shanghai, China) were maintained and cultured as previously described (<a class="elsevierStyleCrossRef" href="#bib16">16</a>).</p></span><span id="cesec60" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle110">Animals</span><p id="para90" class="elsevierStylePara elsevierViewall">Healthy male Balb/c mice (Chongqing Tengxin Biotechnology Co., Ltd., Chongqing, China) were housed under specific pathogen-free conditions. The mice were managed by the Care and Use of Laboratory Animals (NIH Publication No. 85-23, revised 1996), and the Ethics Committee of the First Affiliated Hospital of the Hebei North University approved the experimental design (protocol No: 2019ECHNU033).</p></span><span id="cesec70" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle120">Antibodies</span><p id="para100" class="elsevierStylePara elsevierViewall">The following antibodies were purchased from the respective suppliers: anti-RNPS1 (ab79233), anti-Ki-67 (ab15580), anti-CEA (ab207718), anti-CA199 (ab3982), anti-CA153 (ab109185), anti-HE4 (ab200828), anti-Bcl-2 (ab182858), anti-Bax (ab182733), anti-MLH1 (ab92312), anti-cleaved caspase-3 (ab2302), anti-MSH2 (ab212188), anti-MSH6 (ab92471), and anti-PMS2 (ab110638) (all from Abcam, Cambridge, USA) and anti-β-actin (M01263-2; Boster, Wuhan, China). The secondary antibodies used were anti-rabbit IgG (AS014) and anti-mouse IgG (H+L) (AS003), both from ABclonal (Wuhan, China), and IMR-1A (HY-100431A; MedChemExpress, Dallas, TX, USA).</p></span><span id="cesec80" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle130">RNPS1-knockdown lentivirus administration</span><p id="para110" class="elsevierStylePara elsevierViewall">An <span class="elsevierStyleItalic">RNPS1</span>-knockdown (sh-RNPS1) lentivirus and a control lentivirus (<a class="elsevierStyleCrossRef" href="#tbl1">Table 1</a>) were designed and chemically synthesized (GenePharma Corporation, Shanghai, China) and stored at -80°C. The cells were transduced with the lentiviruses, as previously described (<a class="elsevierStyleCrossRef" href="#bib17">17</a>).</p><elsevierMultimedia ident="tbl1"></elsevierMultimedia><p id="para120" class="elsevierStylePara elsevierViewall">The mice were randomly assigned to the following groups (n=6 per group): control (con), untreated RL952 cells, or mice injected with RL952 cells; sh-RNPS1, RL952 cells transduced with sh-RNPS1 lentivirus or mice injected with RL952 cells infected with sh-RNPS1; lentivirus control (LC)-shRNPS1, lentivirus cells treated with <span class="elsevierStyleItalic">RNPS1</span> control lentivirus, or mice injected with lentivirus cells incubated with <span class="elsevierStyleItalic">RNPS1</span> control lentivirus; and IMR-1A+sh-RNPS1, RL952 cells incubated with sh-RNPS1 lentivirus, or mice injected with RL952 cells incubated with sh-RNPS1 lentivirus or IMR-1A (10 μg <span class="elsevierStyleItalic">in vitro</span> or 10 mg/kg <span class="elsevierStyleItalic">in vivo</span>).</p></span><span id="cesec90" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle140">UCEC mouse model</span><p id="para130" class="elsevierStylePara elsevierViewall">The mice were subcutaneously injected with RL952 cells 5 days later, as previously described (<a class="elsevierStyleCrossRef" href="#bib18">18</a>). The mice were sacrificed when they rapidly lost >20% of their weight and showed signs of deteriorating health, such as hunching, dehydration, and labored breathing due to the metastatic burden.</p></span><span id="cesec100" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle150">Western blotting</span><p id="para140" class="elsevierStylePara elsevierViewall">Proteins (50 μg) from each sample were resolved by 12% SDS-polyacrylamide gel electrophoresis and blotted onto nitrocellulose membranes as previously described (<a class="elsevierStyleCrossRef" href="#bib19">19</a>).</p></span><span id="cesec110" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle160">Immunohistochemistry (IHC)</span><p id="para150" class="elsevierStylePara elsevierViewall">Tissue sections (4-μm-thick) were incubated with primary antibodies against <span class="elsevierStyleItalic">RNPS1</span> and Ki-67 at 4°C overnight, followed by incubation with a secondary antibody, as previously described (<a class="elsevierStyleCrossRef" href="#bib20">20</a>).</p></span><span id="cesec120" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle170">MTT assay</span><p id="para160" class="elsevierStylePara elsevierViewall">After stirring the samples for 30 min, they were passed through a filter with pores (diameter, 0.22 µm), and then stored at 4°C, as previously described (<a class="elsevierStyleCrossRef" href="#bib21">21</a>).</p></span><span id="cesec130" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle180">Statistical analysis</span><p id="para170" class="elsevierStylePara elsevierViewall">Data are expressed as the means±standard deviations and were statistically analyzed by one-way or two-way ANOVA using SPSS version 19.0 (SPSS Inc., Chicago, IL, USA). The Holm-Sidak test was used for multiple comparisons. Statistical significance was set at <span class="elsevierStyleItalic">p</span><0.05.</p></span></span><span id="cesec140" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle190">RESULTS</span><span id="cesec150" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle200">Identifying the potential function of RNPS1 in UCEC using bioinformatics analysis</span><p id="para180" class="elsevierStylePara elsevierViewall"><a class="elsevierStyleCrossRef" href="#fig1">Figure 1</a> shows the predicted role of <span class="elsevierStyleItalic">RNPS1</span> in UCEC detected by TIMER2.0, GSEA, and a Kaplan-Meier plotter. <a class="elsevierStyleCrossRef" href="#fig1">Figure 1A</a> shows that the expression of <span class="elsevierStyleItalic">RNPS1</span>, as determined by TIMER2.0, was higher in UCEC tumors than in normal tissues (<span class="elsevierStyleItalic">p</span><0.05). The GSEA findings (<a class="elsevierStyleCrossRef" href="#fig1">Figure 1B</a>) showed that <span class="elsevierStyleItalic">RNPS1</span> was positively correlated with UCEC progression (<span class="elsevierStyleItalic">p</span><0.05). Analysis of the overall survival (OS) and recurrence-free survival (RFS) indicated that the prognostic outcomes of patients with UCEC and high <span class="elsevierStyleItalic">RNPS1</span> expression (<a class="elsevierStyleCrossRef" href="#fig1">Figure 1C and D</a>) were worse (<span class="elsevierStyleItalic">p</span><0.05).</p><elsevierMultimedia ident="fig1"></elsevierMultimedia></span><span id="cesec160" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle210">Different levels of RNPS1 in tissues or cell lines of UCEC</span><p id="para190" class="elsevierStylePara elsevierViewall">As <span class="elsevierStyleItalic">RNPS1</span> might be involved in UCEC, we analyzed the differences in <span class="elsevierStyleItalic">RNPS1</span> expression among UCEC tissues or cell lines (<a class="elsevierStyleCrossRef" href="#fig2">Figure 2</a>). The <span class="elsevierStyleItalic">RNPS1</span> level was significantly higher in tumors than in para-tumor tissues (<span class="elsevierStyleItalic">p</span><0.05, <a class="elsevierStyleCrossRef" href="#fig2">Figure 2A and B</a>). Similar to the IHC results (<a class="elsevierStyleCrossRef" href="#fig2">Figure 2C</a>), <span class="elsevierStyleItalic">RNPS1</span> was localized in the nucleus. In addition, <span class="elsevierStyleItalic">RNPS1</span> expression was significantly higher in RL952 cells than in other cells (<span class="elsevierStyleItalic">p</span><0.05; <a class="elsevierStyleCrossRef" href="#fig2">Figure 2D and E</a>). Therefore, we used RL952 as the UCEC model cell line associated with <span class="elsevierStyleItalic">RNPS1</span> for further investigation.</p><elsevierMultimedia ident="fig2"></elsevierMultimedia></span><span id="cesec170" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle220">Development of UCEC <span class="elsevierStyleItalic">in vitro</span> was regulated after RNPS1 knockdown</span><p id="para200" class="elsevierStylePara elsevierViewall">We knocked down RNPS1 using the lentivirus sh-RNPS1 to verify the role of RNPS1 in UCEC and its correlation with the previously obtained results (<a class="elsevierStyleCrossRef" href="#fig3">Figure 3</a>). The control, sh-RNPS1, and control-shRNPS1 RL952 cells proliferated (<a class="elsevierStyleCrossRef" href="#fig3">Figure 3A</a>). However, the optical density of the samples, as detected by MTT, decreased at 3 and 4 days in the sh-RNPS1 group (<span class="elsevierStyleItalic">p</span><0.05). We measured the levels of apoptotic and tumor biomarkers of UCEC to determine their regulation after RNPS1 knockdown (<a class="elsevierStyleCrossRef" href="#fig3">Figure 3B</a>). The levels of CEA, CA199, CA153, HE4, and Bcl-2 were reduced, whereas the activities of Bax and cleaved caspase-3 were induced in the sh-RNPS1 group (<span class="elsevierStyleItalic">p</span><0.05, <a class="elsevierStyleCrossRef" href="#fig3">Figure 3C</a>).</p><elsevierMultimedia ident="fig3"></elsevierMultimedia></span><span id="cesec180" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle230">Development of UCEC <span class="elsevierStyleItalic">in vivo</span> was regulated after RNPS1 knockdown</span><p id="para210" class="elsevierStylePara elsevierViewall">As <span class="elsevierStyleItalic">RNPS1</span> knockdown regulated the progress of UCEC <span class="elsevierStyleItalic">in vitro</span>, we examined whether this also occurred <span class="elsevierStyleItalic">in vivo</span> (<a class="elsevierStyleCrossRef" href="#fig4">Figure 4</a>). We found that the tumor volumes of the sh-RNPS1 mice were significantly decreased at 21 and 28 days (<span class="elsevierStyleItalic">p</span><0.05, <a class="elsevierStyleCrossRef" href="#fig4">Figure 4A</a>), and the level of <span class="elsevierStyleItalic">RNPS1</span> and the proliferation index, Ki-67, were reduced (<a class="elsevierStyleCrossRef" href="#fig4">Figure 4B</a>). We assessed the levels of apoptotic and tumor biomarkers in UCECs (<a class="elsevierStyleCrossRef" href="#fig4">Figure 4C</a>). The levels of CEA, CA199, CA153, HE4, and Bcl-2 decreased, while those of Bax and cleaved caspase-3 increased (<span class="elsevierStyleItalic">p</span><0.05, <a class="elsevierStyleCrossRef" href="#fig4">Figure 4F</a>).</p><elsevierMultimedia ident="fig4"></elsevierMultimedia></span><span id="cesec190" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle240">Bioinformatic analyses of the functions of RNPS1 in MSI and MMR in UCEC by pan-cancer, GSEA, and correlation analysis</span><p id="para220" class="elsevierStylePara elsevierViewall"><a class="elsevierStyleCrossRef" href="#fig5">Figure 5A</a> shows the functions of <span class="elsevierStyleItalic">RNPS1</span> and MSI in different types of cancer. We found that <span class="elsevierStyleItalic">RNPS1</span> was positively associated with MSI in the UCEC. The GSEA results showed that <span class="elsevierStyleItalic">RNPS1</span> was negatively for MMR (<a class="elsevierStyleCrossRef" href="#fig5">Figure 5B</a>). Correlation analysis verified that <span class="elsevierStyleItalic">RNPS1</span> was negatively correlated with the MMR markers <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span> but positively correlated with <span class="elsevierStyleItalic">MSH1</span> and <span class="elsevierStyleItalic">PMS2</span> in UCEC (<a class="elsevierStyleCrossRef" href="#fig5">Figure 5B</a>).</p><elsevierMultimedia ident="fig5"></elsevierMultimedia></span><span id="cesec200" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle250">MMR marker levels were increased by RNPS1 knockdown <span class="elsevierStyleItalic">in vivo</span></span><p id="para230" class="elsevierStylePara elsevierViewall">As previous predictions have indicated that the <span class="elsevierStyleItalic">RNPS1</span> gene is associated with MSI and MMR in UCEC, we examined MMR marker levels <span class="elsevierStyleItalic">in vivo</span>. <a class="elsevierStyleCrossRef" href="#fig6">Figure 6A</a> shows the increased expression of <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span> in the sh-RNPS1 group (<span class="elsevierStyleItalic">p</span><0.05) compared with the other groups (<a class="elsevierStyleCrossRef" href="#fig6">Figure 6B</a>).</p><elsevierMultimedia ident="fig6"></elsevierMultimedia></span><span id="cesec210" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle260">Mismatch repair was regulated by RNPS1 knockdown through Notch signaling pathway <span class="elsevierStyleItalic">in vivo</span></span><p id="para240" class="elsevierStylePara elsevierViewall">The GSEA findings showed that <span class="elsevierStyleItalic">RNPS1</span> was positively for Notch, especially, Notch4 signaling (<a class="elsevierStyleCrossRef" href="#fig7">Figure 7A</a>). To confirm this, we blocked Notch expression using an inhibitor of Mastermind Recruitment-1A (IMR-1A). <a class="elsevierStyleCrossRef" href="#fig7">Figure 7B</a> shows that IMR-1A decreased the levels of <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span> after <span class="elsevierStyleItalic">RNPS1</span> knockdown (<span class="elsevierStyleItalic">p</span><0.05) compared with the case in the sh-RNPS1 group (<a class="elsevierStyleCrossRef" href="#fig7">Figure 7C</a>); notably, IMR-1A reduced the <span class="elsevierStyleItalic">RNPS1</span> levels.</p><elsevierMultimedia ident="fig7"></elsevierMultimedia></span><span id="cesec220" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle270">Further bioinformatics analysis of RNPS1 in patients with UCEC using target gene assays</span><p id="para250" class="elsevierStylePara elsevierViewall"><a class="elsevierStyleCrossRef" href="#fig8">Figure S1</a> shows the results of the target gene assays of <span class="elsevierStyleItalic">RNPS1</span> in UCEC tissues. Mutations were found in the group with higher levels of <span class="elsevierStyleItalic">RNPS1, NAA11, C2orf57, NUPR1, GPR157, GTF2H2C, NXNL1, SNCB, FAM177B, RAB29, BCL2L12, PRPH,</span> and <span class="elsevierStyleItalic">WDR74</span>. These results suggest that <span class="elsevierStyleItalic">RNPS1</span> is associated with these gene mutations and participates in the prognosis of UCEC.</p><elsevierMultimedia ident="fig8"></elsevierMultimedia></span></span><span id="cesec230" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle280">DISCUSSION</span><p id="para260" class="elsevierStylePara elsevierViewall">Endometrioid EC is the most common uterine malignancy, with a mortality rate of approximately 20%; it is the most prevalent gynecological malignancy in western and developed countries (<a class="elsevierStyleCrossRef" href="#bib22">22</a>,<a class="elsevierStyleCrossRef" href="#bib23">23</a>). The mortality rates of endometrioid EC are increasing, indicating the need for more effective diagnostic and treatment strategies (<a class="elsevierStyleCrossRef" href="#bib24">24</a>). MMR deficiency due to the loss of MMR protein expression, a hotspot mutation in the POLE exonuclease domain, and a nonspecific molecular profile may be prognostic factors for patients with advanced UCEC (<a class="elsevierStyleCrossRef" href="#bib7">7</a>,<a class="elsevierStyleCrossRef" href="#bib8">8</a>,<a class="elsevierStyleCrossRef" href="#bib25">25</a>).</p><p id="para270" class="elsevierStylePara elsevierViewall">A recent whole-genome analysis found that <span class="elsevierStyleItalic">RNPS1</span> regulates carcinogenesis, especially, in EC (<a class="elsevierStyleCrossRef" href="#bib26">26</a>). As little is known about <span class="elsevierStyleItalic">RNPS1</span>, it should be a hot topic in oncological research. In the present study, bioinformatics and molecular biological methods were applied to determine the functions of <span class="elsevierStyleItalic">RNPS1</span> in UCEC. Higher levels of <span class="elsevierStyleItalic">RNPS1</span> are expressed in UCEC tumors than in normal tissues; the prognostic outcomes of patients with UCEC were poor, and abundant expression of the <span class="elsevierStyleItalic">RNPS1</span> isoform were observed. These results showed that <span class="elsevierStyleItalic">RNPS1</span> may be an oncogene involved in the prognosis of UCEC. To verify this issue, we compared the levels of the <span class="elsevierStyleItalic">RNPS1</span> protein in various tissues and cell lines. The results showed that <span class="elsevierStyleItalic">RNPS1</span> expression was increased in EC tissue and RL952 cells, consistent with the findings of the bioinformatics analyses.</p><p id="para280" class="elsevierStylePara elsevierViewall">Apoptosis is a programmed cell death that does not elicit an inflammatory response (<a class="elsevierStyleCrossRef" href="#bib27">27</a>). Knocking down RNPS1 weakened tumor cell proliferation and biomarkers, reduced tumor volume, increased apoptosis <span class="elsevierStyleItalic">in vitro</span> and <span class="elsevierStyleItalic">in vivo</span>, and inhibited UCEC development in our study. These results showed that RNPS1 could regulate apoptosis and tumor progression in UCEC and were consistent with the findings of the bioinformatics analyses.</p><p id="para290" class="elsevierStylePara elsevierViewall">We further explored the mechanism underlying the action of RNPS1 in EC using bioinformatics methods and found that RNPS1 correlated positively with MSI and negatively with MMR proteins, especially, <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span>. Western blotting confirmed the bioinformatic findings of a relationship between RNPS1 and MMR, as the <span class="elsevierStyleItalic">RNPS1</span> knockdown lentivirus improved the expression of <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span> but not <span class="elsevierStyleItalic">MSH1</span> and <span class="elsevierStyleItalic">PMS2</span>. We plan to report this issue, but some methodological deficiencies resulting from limited laboratory conditions prevent more rigorous and advanced experimentation. Other scholars should investigate these findings further.</p><p id="para300" class="elsevierStylePara elsevierViewall">Clonal diversity was due to the accumulation of mutations in genes of diverse pathways, such as Notch and MMR pathways (<a class="elsevierStyleCrossRef" href="#bib28">28</a>). Notch signaling can provide the first mechanistic example of altered glycosylation in tumor cells with MSI (<a class="elsevierStyleCrossRef" href="#bib29">29</a>). Our GSEA findings showed that <span class="elsevierStyleItalic">RNPS1</span> correlated positively with Notch signaling, especially, the Notch4 signaling pathway in UCEC. We investigated this aspect by blocking Notch signaling using IMR-1A. The results showed that IMR-1A decreased <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span> levels after lentivirus-based <span class="elsevierStyleItalic">RNPS1</span> knockdown. Furthermore, IMR-1A reduced the <span class="elsevierStyleItalic">RNPS1</span> levels, suggesting that Notch is an upstream factor for <span class="elsevierStyleItalic">RNPS1</span>. However, as a specific Notch4 inhibitor is not yet available, we could only inhibit Notch signaling. The present results showed that <span class="elsevierStyleItalic">RNPS1</span> may be a downstream target factor of Notch; therefore, the Notch4 signaling pathway may regulate MMR in UCEC.</p><p id="para310" class="elsevierStylePara elsevierViewall">Bioinformatic analyses of <span class="elsevierStyleItalic">RNPS1</span> in patients with UCEC using the target gene system showed that <span class="elsevierStyleItalic">RNPS1</span> may be associated with mutations in <span class="elsevierStyleItalic">NAA11, C2orf57, NUPR1, GPR157, GTF2H2C, NXNL1, SNCB, FAM177B, RAB29, BCL2L12, PRPH,</span> and <span class="elsevierStyleItalic">WDR74</span>, participating in UCEC prognosis. These data await confirmation in future investigations and will be the focus of our subsequent studies.</p><p id="para320" class="elsevierStylePara elsevierViewall">We found that <span class="elsevierStyleItalic">RNPS1</span> knockdown significantly activated apoptosis and inhibited EC development and <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span> expression <span class="elsevierStyleItalic">via</span> the Notch signaling pathway. Overall, our findings offer a new strategy for treating UCEC.</p></span><span id="cesec240" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle290">AUTHOR CONTRIBUTIONS</span><p id="para330" class="elsevierStylePara elsevierViewall">Liu X designed the study and manuscript drafting. Ma H and Ma L analyzed the data. Li K wrote and revised the manuscript. Kang Y polished the first manuscript drafting and designed the methodology.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:7 [ 0 => array:2 [ "identificador" => "xpalclavsec1577345" "titulo" => "KEYWORDS" ] 1 => array:2 [ "identificador" => "cesec10" "titulo" => "INTRODUCTION" ] 2 => array:3 [ "identificador" => "cesec20" "titulo" => "MATERIALS AND METHODS" "secciones" => array:11 [ 0 => array:2 [ "identificador" => "cesec30" "titulo" => "UCEC specimens from patients" ] 1 => array:2 [ "identificador" => "cesec40" "titulo" => "Bioinformatics analysis" ] 2 => array:2 [ "identificador" => "cesec50" "titulo" => "Cell lines and cell culture" ] 3 => array:2 [ "identificador" => "cesec60" "titulo" => "Animals" ] 4 => array:2 [ "identificador" => "cesec70" "titulo" => "Antibodies" ] 5 => array:2 [ "identificador" => "cesec80" "titulo" => "RNPS1-knockdown lentivirus administration" ] 6 => array:2 [ "identificador" => "cesec90" "titulo" => "UCEC mouse model" ] 7 => array:2 [ "identificador" => "cesec100" "titulo" => "Western blotting" ] 8 => array:2 [ "identificador" => "cesec110" "titulo" => "Immunohistochemistry (IHC)" ] 9 => array:2 [ "identificador" => "cesec120" "titulo" => "MTT assay" ] 10 => array:2 [ "identificador" => "cesec130" "titulo" => "Statistical analysis" ] ] ] 3 => array:3 [ "identificador" => "cesec140" "titulo" => "RESULTS" "secciones" => array:8 [ 0 => array:2 [ "identificador" => "cesec150" "titulo" => "Identifying the potential function of RNPS1 in UCEC using bioinformatics analysis" ] 1 => array:2 [ "identificador" => "cesec160" "titulo" => "Different levels of RNPS1 in tissues or cell lines of UCEC" ] 2 => array:2 [ "identificador" => "cesec170" "titulo" => "Development of UCEC in vitro was regulated after RNPS1 knockdown" ] 3 => array:2 [ "identificador" => "cesec180" "titulo" => "Development of UCEC in vivo was regulated after RNPS1 knockdown" ] 4 => array:2 [ "identificador" => "cesec190" "titulo" => "Bioinformatic analyses of the functions of RNPS1 in MSI and MMR in UCEC by pan-cancer, GSEA, and correlation analysis" ] 5 => array:2 [ "identificador" => "cesec200" "titulo" => "MMR marker levels were increased by RNPS1 knockdown in vivo" ] 6 => array:2 [ "identificador" => "cesec210" "titulo" => "Mismatch repair was regulated by RNPS1 knockdown through Notch signaling pathway in vivo" ] 7 => array:2 [ "identificador" => "cesec220" "titulo" => "Further bioinformatics analysis of RNPS1 in patients with UCEC using target gene assays" ] ] ] 4 => array:2 [ "identificador" => "cesec230" "titulo" => "DISCUSSION" ] 5 => array:2 [ "identificador" => "cesec240" "titulo" => "AUTHOR CONTRIBUTIONS" ] 6 => array:1 [ "titulo" => "REFERENCES" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2021-07-15" "fechaAceptado" => "2021-09-21" "PalabrasClave" => array:1 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "KEYWORDS" "identificador" => "xpalclavsec1577345" "palabras" => array:4 [ 0 => "RNPS1" 1 => "UCEC" 2 => "MMR" 3 => "Proliferation" ] ] ] ] "tieneResumen" => true "resumen" => array:1 [ "en" => array:2 [ "resumen" => "<span id="ceabs10" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle10">OBJECTIVE:</span><p id="spara90" class="elsevierStyleSimplePara elsevierViewall">To determine the role of RNA-binding protein with serine-rich domain 1 (<span class="elsevierStyleItalic">RNPS1</span>) in uterine corpus endometrial carcinoma (UCEC), the role of <span class="elsevierStyleItalic">RNPS1</span> knockdown in UCEC development <span class="elsevierStyleItalic">in vitro</span> and <span class="elsevierStyleItalic">in vivo</span>, and the relationship between <span class="elsevierStyleItalic">RNPS1</span> and mismatch repair (MMR) in UCEC.</p></span> <span id="ceabs20" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle20">METHODS:</span><p id="spara100" class="elsevierStyleSimplePara elsevierViewall">We predicted the potential function of <span class="elsevierStyleItalic">RNPS1</span> using bioinformatics systems. The expression of <span class="elsevierStyleItalic">RNPS1</span> in tissues and cell lines was analyzed by western blotting and immunohistochemistry. The expression of <span class="elsevierStyleItalic">RNPS1</span> in MMR was assessed using bioinformatics and western blotting. The proliferation and apoptosis of UCEC cells were assessed under <span class="elsevierStyleItalic">RNPS1</span> knockdown conditions, and <span class="elsevierStyleItalic">RNPS1</span> regulation in MMR was detected by suppressing Notch signaling. Associations between <span class="elsevierStyleItalic">RNPS1</span> and gene mutations in UCEC and prognosis were analyzed.</p></span> <span id="ceabs30" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle30">RESULTS:</span><p id="spara110" class="elsevierStyleSimplePara elsevierViewall">The <span class="elsevierStyleItalic">RNPS1</span> level was higher in UCEC tumors than in normal tissues and tumors or RL952 cells. Prognostic outcomes were worse when UCEC showed abundant <span class="elsevierStyleItalic">RNPS1</span> expression. Lentiviral <span class="elsevierStyleItalic">RNPS1</span> knockdown weakened tumor cell proliferation and suppressed biomarker expression, reduced the tumor volume, promoted apoptosis <span class="elsevierStyleItalic">in vitro</span> and <span class="elsevierStyleItalic">in vivo</span>, and inhibited UCEC development. Increased MutS homolog 2 (<span class="elsevierStyleItalic">MSH2</span>) and MutS homolog 6 (<span class="elsevierStyleItalic">MSH6</span>) levels in MMR after <span class="elsevierStyleItalic">RNPS1</span> knockdown were reversed by inhibiting Notch signaling. Furthermore, <span class="elsevierStyleItalic">RNPS1</span> was associated with mutations in <span class="elsevierStyleItalic">NAA11</span>, <span class="elsevierStyleItalic">C2orf57</span>, <span class="elsevierStyleItalic">NUPR1</span>, and other genes involved in UCEC prognosis.</p></span> <span id="ceabs40" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="cestitle40">CONCLUSION:</span><p id="spara120" class="elsevierStyleSimplePara elsevierViewall"><span class="elsevierStyleItalic">RNPS1</span> may regulate the expression levels of <span class="elsevierStyleItalic">MSH2</span> and <span class="elsevierStyleItalic">MSH6</span> in MMR, enhancing the proliferation, development, and prognosis of UCEC through a Notch signaling pathway in UCEC. Our study offers a new method and strategy for delaying UCEC development through modulating MMR.</p></span>" "secciones" => array:4 [ 0 => array:2 [ "identificador" => "ceabs10" "titulo" => "OBJECTIVE:" ] 1 => array:2 [ "identificador" => "ceabs20" "titulo" => "METHODS:" ] 2 => array:2 [ "identificador" => "ceabs30" "titulo" => "RESULTS:" ] 3 => array:2 [ "identificador" => "ceabs40" "titulo" => "CONCLUSION:" ] ] ] ] "NotaPie" => array:1 [ 0 => array:1 [ "nota" => "<p class="elsevierStyleNotepara" id="cenpara10">No potential conflict of interest was reported.</p>" ] ] "apendice" => array:1 [ 0 => array:1 [ "seccion" => array:1 [ 0 => array:3 [ "apendice" => "<p id="para340" class="elsevierStylePara elsevierViewall"><elsevierMultimedia ident="fig8"></elsevierMultimedia></p>" "titulo" => "APPENDIX" "identificador" => "cesec250" ] ] ] ] "multimedia" => array:9 [ 0 => array:7 [ "identificador" => "fig1" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1353 "Ancho" => 1753 "Tamanyo" => 294106 ] ] "descripcion" => array:1 [ "en" => "<p id="spara10" class="elsevierStyleSimplePara elsevierViewall">(A) Assessment of <span class="elsevierStyleItalic">RNPS1</span> expression in cancers. (B) GSEA of the correlation between <span class="elsevierStyleItalic">RNPS1</span> and UCEC. (C) OS and (D) RFS analyses of the role of <span class="elsevierStyleItalic">RNPS1</span> in UCEC patients.</p>" ] ] 1 => array:7 [ "identificador" => "fig2" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 765 "Ancho" => 1754 "Tamanyo" => 181096 ] ] "descripcion" => array:1 [ "en" => "<p id="spara20" class="elsevierStyleSimplePara elsevierViewall">(A) <span class="elsevierStyleItalic">RNPS1</span> expression, (B) quantitation of the <span class="elsevierStyleItalic">RNPS1</span> expression levels from the western blots, and (C) IHC staining analysis for <span class="elsevierStyleItalic">RNPS1</span> in para-tumor and tumor tissues (×400). (D) <span class="elsevierStyleItalic">RNPS1</span> expression in NEC, KLE, RL952, Ishikawa, and ECC-1 cells. (E) Quantitation of the <span class="elsevierStyleItalic">RNPS1</span> expression levels in cells. Protein levels were normalized to those of β-actin. (n=6, *<span class="elsevierStyleItalic">p</span><0.05: tumor <span class="elsevierStyleItalic">vs.</span> para-tumor or RL952 <span class="elsevierStyleItalic">vs.</span> other cells).</p>" ] ] 2 => array:7 [ "identificador" => "fig3" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 1605 "Ancho" => 1504 "Tamanyo" => 158110 ] ] "descripcion" => array:1 [ "en" => "<p id="spara30" class="elsevierStyleSimplePara elsevierViewall">(A) Proliferation assays of cells from the Con, sh-RNPS1. and control-shRNPS1 groups at 4 days. (B) Western blots for the analysis of the levels of CEA, CA199, CA153, HE4, Bax, Bcl-2. and cleaved caspase-3. (C) Quantitation of the levels of CEA, CA199, CA153, HE4, Bcl-2, Bax, and cleaved caspase-3. (n=6, *<span class="elsevierStyleItalic">p</span><0.05: sh-RNPS1 <span class="elsevierStyleItalic">vs.</span> other groups).</p>" ] ] 3 => array:7 [ "identificador" => "fig4" "etiqueta" => "Figure 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr4.jpeg" "Alto" => 1296 "Ancho" => 1754 "Tamanyo" => 258865 ] ] "descripcion" => array:1 [ "en" => "<p id="spara40" class="elsevierStyleSimplePara elsevierViewall">(A) Tumor volume in mice from the Con, sh-RNPS1, and control-shRNPS1 groups at 28 days. (B) IHC analysis for detecting the <span class="elsevierStyleItalic">RNPS1</span> levels and Ki-67 index. (C) Western blots for the analysis of the levels of CEA, CA199, CA153, HE4, Bcl-2, Bax, and cleaved caspase-3, (D) Quantitation of the levels of CEA, CA199, CA153, HE4, Bax, Bcl-2, and cleaved caspase-3. (n=6, *<span class="elsevierStyleItalic">p</span><0.05: sh-RNPS1 <span class="elsevierStyleItalic">vs.</span> other groups).</p>" ] ] 4 => array:7 [ "identificador" => "fig5" "etiqueta" => "Figure 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr5.jpeg" "Alto" => 995 "Ancho" => 1503 "Tamanyo" => 135205 ] ] "descripcion" => array:1 [ "en" => "<p id="spara50" class="elsevierStyleSimplePara elsevierViewall">(A) Pan-cancer assays of MSI in different cancers. (B) GSEA of the correlation between <span class="elsevierStyleItalic">RNPS1</span> and MMR in UCEC. (C) Analysis of the correlation of <span class="elsevierStyleItalic">RNPS1</span> with <span class="elsevierStyleItalic">MSH1, MSH2, MSH6,</span> and <span class="elsevierStyleItalic">PMS2</span> in UCEC.</p>" ] ] 5 => array:7 [ "identificador" => "fig6" "etiqueta" => "Figure 6" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr6.jpeg" "Alto" => 694 "Ancho" => 1504 "Tamanyo" => 71017 ] ] "descripcion" => array:1 [ "en" => "<p id="spara60" class="elsevierStyleSimplePara elsevierViewall">(A) Western blots for the analysis of the <span class="elsevierStyleItalic">MSH1, MSH2, MSH6</span>, and <span class="elsevierStyleItalic">PMS2</span> expression levels <span class="elsevierStyleItalic">in vivo</span>, (B) Quantitation of the <span class="elsevierStyleItalic">MSH1, MSH2, MSH6,</span> and <span class="elsevierStyleItalic">PMS2</span> expression levels. (n=6, *<span class="elsevierStyleItalic">p</span><0.05: sh-RNPS1 <span class="elsevierStyleItalic">vs.</span> other groups).</p>" ] ] 6 => array:7 [ "identificador" => "fig7" "etiqueta" => "Figure 7" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr7.jpeg" "Alto" => 871 "Ancho" => 1497 "Tamanyo" => 108089 ] ] "descripcion" => array:1 [ "en" => "<p id="spara70" class="elsevierStyleSimplePara elsevierViewall">(A) GSEA of the correlation between <span class="elsevierStyleItalic">RNPS1</span> and Notch or Notch4 signaling pathway in UCEC. (B) Western blot assay for the analysis of the <span class="elsevierStyleItalic">RNPS1, MSH1, MSH2, MSH6,</span> and <span class="elsevierStyleItalic">PMS2</span> expression levels <span class="elsevierStyleItalic">in vivo</span>. (B) Quantitation of <span class="elsevierStyleItalic">RNPS1, MSH1, MSH2, MSH6,</span> and <span class="elsevierStyleItalic">PMS2</span> expression levels. (n=6, *<span class="elsevierStyleItalic">p</span><0.05: sh-RNPS1 <span class="elsevierStyleItalic">vs.</span> Con; <span class="elsevierStyleSup">#</span><span class="elsevierStyleItalic">p</span><0.05: IMR-1A+sh-RNPS1 <span class="elsevierStyleItalic">vs.</span> sh-RNPS1).</p>" ] ] 7 => array:7 [ "identificador" => "tbl1" "etiqueta" => "Table 1" "tipo" => "MULTIMEDIATABLA" "mostrarFloat" => true "mostrarDisplay" => false "tabla" => array:1 [ "tablatextoimagen" => array:1 [ 0 => array:1 [ "tabla" => array:1 [ 0 => """ <table border="0" frame="\n \t\t\t\t\tvoid\n \t\t\t\t" class=""><thead title="thead"><tr title="table-row"><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Name \t\t\t\t\t\t\n \t\t\t\t\t\t</th><th class="td" title="\n \t\t\t\t\ttable-head\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t" scope="col" style="border-bottom: 2px solid black">Sequence \t\t\t\t\t\t\n \t\t\t\t\t\t</th></tr></thead><tbody title="tbody"><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">sh-RNPS1-421 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5′-taataaaaagtccagcacta-3′ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">sh-RNPS1-601 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5′-tcggtccagctcgacttcca-3′ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">sh-RNPS1-1262 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5′-cgctccagctccaactcctc-3′ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Negative Control \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5′-ataccccacccagctcagtt-3′ \t\t\t\t\t\t\n \t\t\t\t</td></tr><tr title="table-row"><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">Control-shRNPS1 \t\t\t\t\t\t\n \t\t\t\t</td><td class="td" title="\n \t\t\t\t\ttable-entry\n \t\t\t\t " align="left" valign="\n \t\t\t\t\ttop\n \t\t\t\t">5′-ttgtcacttttctagccaaa-3′ \t\t\t\t\t\t\n \t\t\t\t</td></tr></tbody></table> """ ] ] ] ] "descripcion" => array:1 [ "en" => "<p id="spara80" class="elsevierStyleSimplePara elsevierViewall">Sequences of RNPS1 lentiviruses.</p>" ] ] 8 => array:7 [ "identificador" => "fig8" "etiqueta" => "Figure S1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => false "mostrarDisplay" => true "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr8.jpeg" "Alto" => 2256 "Ancho" => 1753 "Tamanyo" => 371766 ] ] "descripcion" => array:1 [ "en" => "<p id="spara130" class="elsevierStyleSimplePara elsevierViewall">(A) Expression of <span class="elsevierStyleItalic">RNPS1</span> in UCEC patients with mutant or wild-type <span class="elsevierStyleItalic">NAA11</span>, <span class="elsevierStyleItalic">C2orf57</span>, <span class="elsevierStyleItalic">NUPR1</span>, <span class="elsevierStyleItalic">GPR157</span>, <span class="elsevierStyleItalic">GTF2H2C</span>, <span class="elsevierStyleItalic">NXNL1</span>, <span class="elsevierStyleItalic">SNCB</span>, <span class="elsevierStyleItalic">FAM177B</span>, <span class="elsevierStyleItalic">RAB29</span>, <span class="elsevierStyleItalic">BCL2L12</span>, <span class="elsevierStyleItalic">PRPH</span>, and <span class="elsevierStyleItalic">WDR74</span>.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "REFERENCES" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "cebibsec10" "bibliografiaReferencia" => array:29 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Identification of a Multi-RNA-Type-Based Signature for Recurrence-Free Survival Prediction in Patients with Uterine Corpus Endometrial Carcinoma" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:5 [ 0 => """ P Wang \n \t\t\t\t\t\t\t\t """ 1 => """ Z Zeng \n \t\t\t\t\t\t\t\t """ 2 => """ X Shen \n \t\t\t\t\t\t\t\t """ 3 => """ X Tian \n \t\t\t\t\t\t\t\t """ 4 => """ Q Ye \n \t\t\t\t\t\t\t\t """ ] ] ] ] ] "host" => array:2 [ 0 => array:2 [ "doi" => "10.1089/dna.2019.5148" "Revista" => array:7 [ "tituloSerie" => "DNA Cell Biol" "fecha" => "2020" "volumen" => "39" "numero" => "4" "paginaInicial" => 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2024 June | 23 | 17 | 40 |
2024 May | 28 | 14 | 42 |
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2024 March | 52 | 19 | 71 |
2024 February | 67 | 16 | 83 |
2024 January | 27 | 16 | 43 |
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2023 August | 32 | 8 | 40 |
2023 July | 21 | 24 | 45 |
2023 June | 20 | 7 | 27 |
2023 May | 47 | 1 | 48 |
2023 April | 39 | 2 | 41 |
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