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首页> 外文期刊>Molecular medicine reports >microRNA-630 promotes cell proliferation and inhibits apoptosis in the HCT116 human colorectal cancer cell line
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microRNA-630 promotes cell proliferation and inhibits apoptosis in the HCT116 human colorectal cancer cell line

机译：MicroRNA-630促进细胞增殖并抑制HCT116人结肠直肠癌细胞系中的细胞凋亡

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摘要

Dysregulation of microRNAs (miRNAs) in colorectal cancer provides important opportunities for the development of future miRNA-based therapies. The present study aimed to assess the role of miRNA-630 (miR-630) expression in colorectal cancer. HCT116 human colorectal cancer cells were transfected with miR-630 inhibitor, mimic or control miRNA, and the effects of miR-630 dysregulation on cell viability, proliferation and apoptosis were analyzed using MTT and bromodeoxyuridine assays, and an annexin V-fluorescein isothiocyanate cell apoptosis kit, respectively. In addition, the changes in the protein expression of proliferation-associated and AKT signaling pathway proteins were analyzed by western blot analysis. The results of the present study demonstrated that overexpression of miR-630 significantly promoted HCT116 cell proliferation however inhibited apoptosis. Furthermore, miR-630 overexpression reduced the protein expression of p27, BCL2-associated X apoptosis regulator, procaspase-3 and active caspase-3, and increased the levels of phosphorylated-AKT and BCL2 apoptosis regulator. The suppression of miR-630 led to the opposite results. In conclusion, the present findings suggested that miR-630 may function as an oncogenic miRNA in colorectal cancer, and may promote cellular proliferation and inhibit apoptosis, through the regulation of the expression of p27 and the AKT signaling pathway. The present study suggested that the inhibition of miR-630 may have potential as an alternative therapeutic strategy for the treatment of patients with colorectal cancer.
机译：细胞癌中微小ROGARAS（miRNA）的缺点为未来的MiRNA疗法提供了重要机会。本研究旨在评估miRNA-630（miR-630）表达在结肠直肠癌中的作用。用miR-630抑制剂，模拟或对照miRNA转染HCT116人结肠直肠癌细胞，使用MTT和溴酰基尿苷测定分析MiR-630失调对细胞活力，增殖和细胞凋亡的影响，以及膜蛋白V-FlyoRece in等硫氰酸酯细胞凋亡套件分别。此外，通过Western印迹分析分析了蛋白质表达的增殖相关和Akt信号传导途径蛋白的变化。本研究的结果表明，MIR-630的过度表达显着促进了HCT116细胞增殖，但抑制细胞凋亡。此外，MIR-630过表达降低了P27，BCL2相关X凋亡调节剂，Procaspase-3和活性Caspase-3的蛋白质表达，并增加了磷酸化-AKT和BCL2凋亡调节剂的水平。 MIR-630的抑制导致了相反的结果。总之，本研究结果表明，MIR-630可以作为结直肠癌的致癌miRNA，并且可以通过调节P27和AKT信号通路的表达来促进细胞增殖和抑制细胞凋亡。本研究表明，MIR-630的抑制可能具有潜在的替代治疗患者的结直肠癌患者。

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