Jiang Hong-Lei, Yu Hao, Ma Xu, Xu Dong, Lin Guo-Fu, Ma Dong-Yan, Jin Jun-Zhe
The Fourth Affiliated Hospital of China Medical University, Shenyang, China.
Tumour Biol. 2014 Jul;35(7):6955-60. doi: 10.1007/s13277-014-1933-x. Epub 2014 Apr 17.
Multiple studies have shown that steroid receptor coactivator-3 (SRC-3) is upregulated and promotes cell proliferation in several human cancers, including breast, lung, and prostate carcinoma. However, its molecular determinants remain largely unexplored. In the current study, by way of informatics software, we found that MicroRNA-195 (miR-195) could negatively regulate protein levels of SRC-3 through targeting its 3'-untranslated region (3'-UTR) in hepatocellular carcinoma (HCC) cells. As a result, miR-195 mimics inhibited while its antisense enhanced SRC-3 protein levels. Furthermore, miR-195 could modulate cell proliferation and tumor growth in vivo and in vitro. Therefore, our results demonstrate a novel molecular mechanism for the dysregulated expression of SRC-3 in hepatocellular carcinoma.
多项研究表明，类固醇受体共激活因子-3（SRC-3）在包括乳腺癌、肺癌和前列腺癌在内的多种人类癌症中表达上调并促进细胞增殖。然而，其分子决定因素在很大程度上仍未得到探索。在当前的研究中，通过信息学软件，我们发现MicroRNA-195（miR-195）可以通过靶向肝细胞癌（HCC）细胞中的3'-非翻译区（3'-UTR）来负调控SRC-3的蛋白水平。因此，miR-195模拟物抑制而其反义物增强了SRC-3蛋白水平。此外，miR-195可以在体内和体外调节细胞增殖和肿瘤生长。因此，我们的结果证明了肝细胞癌中SRC-3表达失调的一种新的分子机制。
