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miR-646 通过抑制 FGF2 和 CCND2 抑制非小细胞肺癌的增殖和转移。

MiR-646 suppresses proliferation and metastasis of non-small cell lung cancer by repressing FGF2 and CCND2.

机构信息

Department of Respiratory Disease, Jinshan Hospital of Fudan University, Shanghai, China.

Xuanqiao Community Health Service Center, Shanghai, China.

出版信息

Cancer Med. 2020 Jun;9(12):4360-4370. doi: 10.1002/cam4.3062. Epub 2020 Apr 29.

Abstract

MicroRNA-646 (miR-646) has been implicated in several other cancers; however, its functional mechanism in non-small cell lung cancer (NSCLC) remains unclear. In this study, we observed the downregulation of miR-646 expression in NSCLC tissues and cell lines. Low-level expression of miR-646 was associated with metastasis and stage of NSCLCs. Functional assays showed that overexpression of miR-646 could suppress NSCLC cell proliferation, clonogenicity, invasion, and inhibit epithelial-mesenchymal transition (EMT), whereas decreased miR-646 expression showed the opposite effects. Importantly, miR-646 overexpression attenuated in vivo tumor growth and metastasis in nude mice models. Mechanically, miR-646 directly targeted and suppressed fibroblast growth factor 2 (FGF2) and cyclin D2 (CCND2) expression. Reintroduction of FGF2 and CCND2 attenuated miR-646-mediated suppression of proliferation and invasion in NSCLC. Collectively, these results demonstrate that miR-646 acts as a tumor suppressor in NSCLC by targeting FGF2 and CCND2, and may serve as a therapeutic target for patients with NSCLC.

摘要

微小 RNA-646(miR-646)已被牵涉到多种其他癌症中;然而,其在非小细胞肺癌(NSCLC)中的功能机制仍不清楚。在本研究中,我们观察到 miR-646 在 NSCLC 组织和细胞系中的表达下调。miR-646 的低水平表达与 NSCLC 的转移和分期相关。功能分析表明,miR-646 的过表达可抑制 NSCLC 细胞的增殖、集落形成、侵袭,并抑制上皮-间充质转化(EMT),而降低 miR-646 的表达则表现出相反的效果。重要的是,miR-646 的过表达在裸鼠模型中减弱了体内肿瘤的生长和转移。在机制上,miR-646 直接靶向并抑制成纤维细胞生长因子 2(FGF2)和周期蛋白 D2(CCND2)的表达。FGF2 和 CCND2 的再引入减弱了 miR-646 对 NSCLC 增殖和侵袭的抑制作用。综上所述,这些结果表明,miR-646 通过靶向 FGF2 和 CCND2 发挥 NSCLC 中的肿瘤抑制作用,可能成为 NSCLC 患者的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0ef/7300416/1b311693617b/CAM4-9-4360-g001.jpg

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