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首页> 外文期刊>European review for medical and pharmacological sciences. >LncRNA ROR promotes proliferation of endometrial cancer cells via regulating Notch1 pathway
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LncRNA ROR promotes proliferation of endometrial cancer cells via regulating Notch1 pathway

机译:通过调节Notch1途径促进子宫内膜癌细胞的增殖促进子宫内膜癌细胞的增殖

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OBJECTIVE: The aim of this study was to investigate the effects of long non-coding ribonucleic acid regulator of reprogramming (lncRNA ROR) on the proliferation and apoptosis of endometrial cancer (EC) cells, and to explore its possible underlying mechanism. PATIENTS AND METHODS: The expression levels of lncRNA ROR and Notch1 in EC tissues were detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The changes in Notch1 protein were detected via Western blotting. Subsequently, the regulatory mechanism of lncRNA ROR on Notch1 was analyzed using Luciferase reporter gene assay. Moreover, the changes in cell proliferation and apoptosis were determined through cell counting kit-8 (CCK-8) assay and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay, respectively. RESULTS: Both lncRNA ROR and Notch1 were highly expressed in EC tissues (p0.05). After overexpression of lncRNA ROR, HEC-1A cells had significantly enhanced proliferation (p0.05) and weakened apoptosis (p0.05). Meanwhile, the mRNA and protein levels of Notch1 rose remarkably compared with those in control group (p0.05). Luciferase reporter gene assay revealed that lncRNA ROR could bind to the Notch1 regulatory factor miR-34a and inhibit its activity. CONCLUSIONS: LncRNA ROR regulates the proliferation and apoptosis of EC cells via promoting the expression of Notch1 protein.
机译:目的:本研究的目的是探讨长期非编码核糖核酸调节剂重编程(LNCRNA ROR)对子宫内膜癌(EC)细胞的增殖和凋亡的影响,并探讨其可能的潜在机制。患者和方法:通过定量逆转录聚合酶链反应(QRT-PCR)检测EC组织中LNCRNA ROR和NOTCH1的表达水平。通过蛋白质印迹检测Notch1蛋白的变化。随后,使用荧光素酶报告基因测定分析LNCRNA ROR对NOTCH1的调节机制。此外,通过细胞计数试剂盒-8(CCK-8)测定和末端脱氧核苷酸转移酶介导的DUTP缺口末端标记(TUNEL)测定,测定细胞增殖和细胞凋亡的变化。结果:LNCRNA ROR和NOTCH1在EC组织中高度表达(P <0.05)。在过表达LNCRNA ROR后,HEC-1A细胞具有显着增强的增殖(P <0.05)并削弱了凋亡(P <0.05)。同时,与对照组中的Notch1的mRNA和蛋白质水平显着上升(P <0.05)。荧光素酶报告基因测定显示LNCRNA ROR可以与Notch1调节因子miR-34a结合并抑制其活性。结论:LNCRNA ROR通过促进Notch1蛋白的表达来调节EC细胞的增殖和凋亡。

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