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首页> 外文期刊>European review for medical and pharmacological sciences. >Effects of LncRNA KCNQ1OT1 on proliferation and migration of ovarian cancer cells by Wnt/β-catenin
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Effects of LncRNA KCNQ1OT1 on proliferation and migration of ovarian cancer cells by Wnt/β-catenin

机译:LNCRNA KCNQ1OT1对WNT /β-catenin的卵巢癌细胞增殖和迁移的影响

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OBJECTIVE: To explore the role of long noncoding ribonucleic acid (lncRNA) KCNQ1OT1 in the proliferation, apoptosis, and migration of ovarian cancer cells via Wnt/β-catenin. MATERIALS AND METHODS: Ovarian cancer A2780 cells were divided into three groups, namely control group, KCNQ1OT1 overexpression group, and KCNQ1OT1 knockdown group. Next, the effect of KCNQ1OT1 on the proliferation of ovarian cancer A2780 cells was detected by cell counting kit-8 (CCK-8) assay. Wound healing assay and transwell assay were carried out to determine the influence of KCNQ1OT1 on the migration ability of ovarian cancer A2780 cells. The role of KCNQ1OT1 in the cell cycle of ovarian cancer A2780 cells was detected via flow cytometry. The impact of KCNQ1OT1 on the expression level of β-catenin protein in ovarian cancer A2780 cells was determined through Western blotting and fluorescence immunoassay. RESULTS: The proliferation rate of cells was overtly decreased in KCNQ1OT1 knockdown group but significantly increased in KCNQ1OT1 overexpression group. The results of both wound healing and transwell assays showed that the migration ability of cells was reduced in KCNQ1OT1 knockdown group but raised in KCNQ1OT1 overexpression group. According to flow cytometry, the cell cycle was clearly arrested in the G0/G1 phase in KCNQ1OT1 knockdown group. The results of Western blotting and fluorescence immunoassay revealed that compared with that in control group, the expression level of β-catenin protein evidently declined in KCNQ1OT1 knockdown group, but it was notably elevated in KCNQ1OT1 overexpression group. CONCLUSIONS: Increased lncRNA KCNQ1OT1 in ovarian cancer cells promotes the expression of β-catenin, thereby facilitating the proliferation and migration of ovarian cancer cells.
机译:目的:探讨长度非致核核酸(LNCRNA)KCNQ101在卵巢癌细胞通过WNT /β-catenin的增殖,细胞凋亡和迁移的作用。材料和方法:卵巢癌A2780细胞分为三组,即对照组,KCNQ1OT1过表达组和KCNQ1OT1敲低组。接下来,通过细胞计数试剂盒-8(CCK-8)测定检测KCNQ1OT1对卵巢癌A2780细胞增殖的影响。进行伤口愈合测定和Transwell测定以确定KCNQ1OT1对卵巢癌A2780细胞迁移能力的影响。通过流式细胞术检测KCNQ1OT1在卵巢癌A2780细胞细胞周期中的作用。通过蛋白质印迹和荧光免疫测定,测定KCNQ1OT1对卵巢癌A2780细胞中β-catenin蛋白表达水平的影响。结果:KCNQ1OT1敲低组细胞的增殖率明显降低,但在KCNQ1OT1过表达组中显着增加。伤口愈合和翻转测定的结果表明,KCNQ1OT1敲低组中细胞的迁移能力降低,但在KCNQ1OT1过表达组中提出。根据流式细胞术,细胞周期在KCNQ1OT1敲低基团中的G0 / G1相中清楚地被捕。 Western印迹和荧光免疫测定结果显示,与对照组中的β-连环蛋白蛋白的表达水平明显下降,但在KCNQ1OT1过表达组中显着升高。结论:卵巢癌细胞中LNCRNA KcNQ1OT1增加促进β-catenin的表达,从而促进卵巢癌细胞的增殖和迁移。

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