Xiang Jie, Hang Jun-Biao, Che Jia-Ming, Li He-Cheng
Department of Thoracic Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai 200025, China.
Int J Clin Exp Pathol. 2015 Aug 1;8(8):9147-53. eCollection 2015.
Increasing evidence showed that miR-25 is involved in the carcinogenesis and progression of various human cancers, while its role in non-small cell lung cancer (NSCLC) is still unclear. Here, we found that miR-25 is significantly up-regulated in NSCLC tissue samples and cell lines. Inhibition of miR-25 remarkably suppressed cell proliferation, migration and invasion in NSCLC cells, whereas enforced expression of miR-25 significantly increased NSCLC cells proliferation, migration and invasion. Moreover, we identified F-box and WD repeat domain-containing 7 (FBXW7) as a direct target of miR-25 and overexpression of FBXW7 partially attenuates the oncogenic effect of miR-25 on NSCLC cells. In conclusion, miR-25 is up-regulated in NSCLC and promotes NSCLC cells proliferation and motility partially by targeting FBXW7. Our data suggest that miR-25 might serve as a potential therapeutic target for NSCLC treatment in the future.
越来越多的证据表明，miR-25参与了多种人类癌症的发生和发展，但其在非小细胞肺癌（NSCLC）中的作用仍不清楚。在此，我们发现miR-25在NSCLC组织样本和细胞系中显著上调。抑制miR-25可显著抑制NSCLC细胞的增殖、迁移和侵袭，而强制表达miR-25则显著增加NSCLC细胞的增殖、迁移和侵袭。此外，我们确定含F盒和WD重复结构域7（FBXW7）是miR-25的直接靶点，FBXW7的过表达部分减弱了miR-25对NSCLC细胞的致癌作用。总之，miR-25在NSCLC中上调，并通过靶向FBXW7部分促进NSCLC细胞的增殖和运动。我们的数据表明，miR-25可能在未来作为NSCLC治疗的潜在靶点。
