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Lentivirus-mediated knockdown of NOB1 suppresses the proliferation of colon cancer cells

机译:慢病毒介导的NOB1敲低抑制结肠癌细胞的增殖

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NOB1 is important for ribosome biogenesis and protein degradation. Previous studies showed that it could regulate the growth and colony-formation ability of ovarian, breast and hepatocellular carcinoma cells. However, its function in colon cancer cells is largely unknown. In this study, we found that NOB1 could express in 6 different colon cancer cell lines. Lentivirus-mediated shRNA targeted NOB1 could suppress the endogenous gene expression. NOB1 depletion significantly inhibited cell proliferation and colony formation ability, as determined by MTT and colony formation assays. Flow cytometry analysis showed NOB1 silencing arrested cell cycle in G0 / G1 phase. Moreover, the percentage of cells at sub-G1 phase dramatically increased after NOB1 knockdown. These results indicate that NOB1 may play an important role in the growth and tumorigensis of colon cancer and knockdown of NOB1 may be a potential therapeutic method for colon cancer in the future.
机译:NOB1对于核糖体的生物发生和蛋白质降解很重要。先前的研究表明,它可以调节卵巢,乳腺癌和肝细胞癌细胞的生长和集落形成能力。然而,其在结肠癌细胞中的功能很大程度上未知。在这项研究中,我们发现NOB1可以在6种不同的结肠癌细胞系中表达。慢病毒介导的shRNA靶向NOB1可以抑制内源基因表达。如MTT和集落形成试验所确定的,NOB1消耗显着抑制细胞增殖和集落形成能力。流式细胞仪分析显示,NOB1沉默使G0 / G1期细胞停滞。而且,NOB1敲低后,sub-G1期的细胞百分比急剧增加。这些结果表明,NOB1可能在结肠癌的生长和肿瘤中起重要作用,而敲除NOB1可能是将来结肠癌的一种潜在治疗方法。

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