miR-187 通过靶向 FGF9 抑制非小细胞肺癌细胞增殖。
MiR-187 suppresses non-small-cell lung cancer cell proliferation by targeting FGF9.
机构信息
Department of Respiratory, HeXian Memorial Hospital Affiliated with Southern Medical University, Guang zhou, China.
GuangZhou Chest Hospital, Guang zhou, China.
出版信息
Bioengineered. 2020 Dec;11(1):70-80. doi: 10.1080/21655979.2019.1706287.
Non-small-cell lung cancer (NSCLC) is the main pathological type of lung cancer and has a low overall five-year survival rate. miR-187 has been reported to play major roles in various tumor types. In this study, we explored the impact of miR-187 on NSCLC. qRT-PCR results demonstrated that miR-187 expression is lower in NSCLC and cancer cells than normal tissues and normal lung cells. miR-187 expression levels are associated with tumor size, TNM stage and overall survival rate. MTS and colony formation assays showed that high miR-187 expression inhibits NSCLC cell proliferation and colony formation ability, and flow cytometry showed that miR-187 overexpression induces cell cycle arrest at the G0/G1 phase. A luciferase reporter assay showed that FGF9 is a target of miR-187. miR-187 overexpression reduces the expression of FGF9, cyclin D1 CDK4 and CDK6. Therefore, miR-187 may present a new NSCLC treatment target by regulates cyclins-related protein expression.
非小细胞肺癌（NSCLC）是肺癌的主要病理类型，总体五年生存率较低。miR-187 已被报道在多种肿瘤类型中发挥重要作用。在本研究中，我们探讨了 miR-187 对 NSCLC 的影响。qRT-PCR 结果表明，miR-187 在 NSCLC 和癌细胞中的表达低于正常组织和正常肺细胞。miR-187 的表达水平与肿瘤大小、TNM 分期和总生存率相关。MTS 和集落形成实验表明，高 miR-187 表达抑制 NSCLC 细胞的增殖和集落形成能力，流式细胞术表明 miR-187 过表达诱导细胞周期停滞在 G0/G1 期。荧光素酶报告基因实验表明，FGF9 是 miR-187 的靶基因。miR-187 过表达降低了 FGF9、cyclin D1、CDK4 和 CDK6 的表达。因此，miR-187 可能通过调节 cyclins 相关蛋白的表达成为 NSCLC 的新治疗靶点。
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