Department of Respiratory Medicine, Jining NO.1 People's Hospital, Jining 272011, China.
Department of tuberculousis, Jining Infectious Disease Hospital, Jining 272031, China.
Biomed Pharmacother. 2017 Nov;95:497-503. doi: 10.1016/j.biopha.2017.08.052. Epub 2017 Sep 12.
Lung cancer is the leading cause of worldwide cancer-related deaths, although many drugs and new therapeutic approaches have been used, the 5-years survival rate is still low for lung cancer patients. microRNAs have been shown to regulate lung cancer initiation and development, here we studied the role of miR-3607 in lung cancer cell proliferation. We found miR-3607 was upregulated in lung cancer tissues and cells, miR-3607 overexpression promoted lung cancer cell A549 proliferation determined by MTT assay, colony formation assay, anchorage-independent growth ability assay and bromodeoxyuridine incorporation assay, while the opposite phenotypes were shown when miR-3607 was knocked down. Predicted analysis suggested a Wnt signaling pathway regulator adenomatous polyposis coli (APC) was the target of miR-3607, miR-3607 could directly bind to the 3'UTR of APC, and promoted Cyclin D1 and c-Myc expression which can be suppressed by APC. Double knockdown of miR-3607 and APC copied the phenotypes of miR-3607 overexpression, suggesting miR-3607 promoted lung cancer cell A549 proliferation by targeting APC. In conclusion, our study suggested miR-3607 contributes to lung cancer cell proliferation by inhibiting APC.
肺癌是全球癌症相关死亡的主要原因，尽管已经使用了许多药物和新的治疗方法，但肺癌患者的 5 年生存率仍然很低。microRNAs 已被证明可以调节肺癌的发生和发展，在这里我们研究了 miR-3607 在肺癌细胞增殖中的作用。我们发现 miR-3607 在肺癌组织和细胞中上调，miR-3607 的过表达通过 MTT 测定、集落形成测定、非依赖性生长能力测定和溴脱氧尿苷掺入测定确定促进肺癌细胞 A549 的增殖，而当 miR-3607 被敲低时则表现出相反的表型。预测分析表明，Wnt 信号通路调节剂腺瘤性结肠息肉病基因（APC）是 miR-3607 的靶标，miR-3607 可以直接结合 APC 的 3'UTR，并促进细胞周期蛋白 D1 和 c-Myc 的表达，而 APC 可以抑制其表达。miR-3607 和 APC 的双重敲低复制了 miR-3607 过表达的表型，表明 miR-3607 通过靶向 APC 促进肺癌细胞 A549 的增殖。总之，我们的研究表明，miR-3607 通过抑制 APC 促进肺癌细胞的增殖。
