Park Sungjin, Minai-Tehrani Arash, Xu Cheng-Xiong, Chang Seung-Hee, Woo Min-Ah, Noh Mi-Suk, Lee Eun-Sun, Lim Hwang-Tae, An Gil-Hwan, Lee Kee-Ho, Sung Ha-Jung, Beck George R, Cho Myung-Haing
Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea.
Mol Med Rep. 2010 Nov-Dec;3(6):1007-13. doi: 10.3892/mmr.2010.373. Epub 2010 Sep 27.
Let-7g miRNAs, short non-coding RNAs approximately 21 nucleotides long, repress protein translation by binding to the 3'UTR of target mRNAs. Aberrant expression of let-7g is associated with the poor prognosis of lung cancer patients. Compared to normal lung cells, let-7g expression is absent in non-small cell lung cancer (NSCLC) cells. Furthermore, K-Ras and HMGA2 are well known as targets of let-7g. In this study, we evaluated the potential role of precursor (pre)-let-7g in lung cancer cell metastasis, focusing on the two targets of let-7g, HMGA2 and K-Ras. We found that pre-let-7g inhibited the migration of A549 lung cancer cells through HMGA2-mediated E2F1 down-regulation. Thus, our results suggest that pre-let-7g could be used as a suitable target for the suppression of lung cancer cell migration.
Let-7g微小RNA是长度约为21个核苷酸的短链非编码RNA，通过与靶mRNA的3'非翻译区（3'UTR）结合来抑制蛋白质翻译。Let-7g的异常表达与肺癌患者的不良预后相关。与正常肺细胞相比，非小细胞肺癌（NSCLC）细胞中不存在Let-7g表达。此外，K-Ras和HMGA2是众所周知的Let-7g靶标。在本研究中，我们评估了前体（pre）-Let-7g在肺癌细胞转移中的潜在作用，重点关注Let-7g的两个靶标HMGA2和K-Ras。我们发现pre-let-7g通过HMGA2介导的E2F1下调抑制了A549肺癌细胞的迁移。因此，我们的结果表明pre-let-7g可作为抑制肺癌细胞迁移的合适靶点。
