首页> 外文期刊>Medical science monitor : >MicroRNA-455-3p Inhibits Tumor Cell Proliferation and Induces Apoptosis in HCT116 Human Colon Cancer Cells
【24h】

MicroRNA-455-3p Inhibits Tumor Cell Proliferation and Induces Apoptosis in HCT116 Human Colon Cancer Cells

机译:MicroRNA-455-3p在HCT116人结肠癌细胞中抑制肿瘤细胞增殖并诱导凋亡

获取原文
           

摘要

BACKGROUND MicroRNAs have been reported to play significant roles in pathogenesis of colorectal cancer (CRC). In the present study, we aimed to investigate the functional role of microRNA-455-3p (miR-455-3p) in CRC, as well as its underlying mechanisms. MATERIAL AND METHODS Human colon cancer cell line HCT116 cells were transfected with miR-455-3p mimics, inhibitors, or controls. After transfection, the effects of miR-455-3p mimics or inhibitors on cell proliferation were analyzed by 3-(4, 5-dimethyl-2- thiazolyl)-2, 5-diphenyl -2-H-tetrazolium bromide (MTT) assay and BrdU assay, and the effects of miR-455-3p mimics or inhibitors on cell apoptosis were determined. In addition, the underlying mechanisms of cell proliferation and apoptosis were explored by assessing the protein levels of cell cycle regulators and apoptosis-related protein. RESULTS The results showed that overexpression of miR-455-3p significantly inhibited the cell proliferation ([i]P[/i]<0.05 or <0.01) in HCT116 cells compared with the control group, but significantly increased the apoptosis ([i]P[/i]<0.01). On the contrary, suppression of miR-455-3p significantly increased the cell proliferation but decreased the apoptosis. Moreover, we found that overexpression of miR-455-3p significantly elevated the protein levels of p27 kinase inhibition protein (KIP) 1, Bax, pro-caspase-3, and active caspase-3, and markedly downregulated the levels of B-cell lymphoma-2 (Bcl-2). Contrary results were found by suppression of miR-455-3p. However, there were no significant differences in p21 expression. CONCLUSIONS MiRNA-455-3p functions as an anti-oncogene in HCT116 cells by inhibiting cell proliferation and inducing of apoptosis.
机译:背景技术据报道,微小RNA在大肠癌(CRC)的发病机理中起重要作用。在本研究中,我们旨在研究microRNA-455-3p(miR-455-3p)在CRC中的功能及其潜在机制。材料与方法用miR-455-3p模拟物,抑制剂或对照转染人结肠癌细胞HCT116细胞。转染后,通过3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-溴化四唑(MTT)分析分析miR-455-3p模拟物或抑制剂对细胞增殖的影响。和BrdU分析,并确定miR-455-3p模拟物或抑制剂对细胞凋亡的影响。此外,通过评估细胞周期调节因子和凋亡相关蛋白的蛋白水平,探索了细胞增殖和凋亡的潜在机制。结果结果表明,与对照组相比,miR-455-3p的过表达显着抑制了HCT116细胞的细胞增殖([i] P [/ i] <0.05或<0.01),但显着增加了细胞凋亡([i] P [/ i] <0.01)。相反,miR-455-3p的抑制显着增加了细胞增殖,但降低了细胞凋亡。此外,我们发现miR-455-3p的过表达显着提高了p27激酶抑制蛋白(KIP)1,Bax,pro-caspase-3和active caspase-3的蛋白水平,并显着下调了B细胞的水平淋巴瘤2(Bcl-2)。通过抑制miR-455-3p发现了相反的结果。但是,p21表达没有显着差异。结论MiRNA-455-3p通过抑制细胞增殖和诱导细胞凋亡,在HCT116细胞中起抗癌基因的作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号