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LINC00152通过mTOR信号通路靶向EpCAM促进肝细胞癌增殖。

LINC00152 promotes proliferation in hepatocellular carcinoma by targeting EpCAM via the mTOR signaling pathway.

作者信息

Ji Jie, Tang Junwei, Deng Lei, Xie Yu, Jiang Runqiu, Li Guoqiang, Sun Beicheng

机构信息

Liver Transplantation Center of The First Affiliated Hospital and Collaborative Innovation Center For Cancer Personalized Medicine, Nanjing Medical University, Nanjing, Jiangsu Province, P.R. China.

出版信息

Oncotarget. 2015 Dec 15;6(40):42813-24. doi: 10.18632/oncotarget.5970.

Abstract

Hepatocellular carcinoma (HCC) is well known as the sixth most common malignant tumor and the third leading cause of cancer-related deaths globally. LINC00152 was documented as an important long non-coding RNA (lncRNA) involved in the pathogenesis of gastric cancer; however, the detailed mechanism of action of LINC00152 remains unknown. Here, based on the increased level of LINC00152 in HCC tissues, we found that LINC00152 could promote cell proliferation in vitro and tumor growth in vivo. Furthermore, microarray-based analysis indicated that LINC00152 could activate the mechanistic target of rapamycin(mTOR) pathway by binding to the promoter of EpCAM through a cis-regulation, as confirmed by Gal4-λN/BoxB reporter system. Thus, LINC00152 might be involved in the oncogenesis of HCC by activating the mTOR signaling pathway and might be a novel index for clinical diagnosis in the future.

摘要

肝细胞癌(HCC)是全球第六大常见恶性肿瘤,也是癌症相关死亡的第三大主要原因。LINC00152被证明是一种参与胃癌发病机制的重要长链非编码RNA(lncRNA);然而,LINC00152的详细作用机制仍不清楚。在此,基于肝癌组织中LINC00152水平的升高,我们发现LINC00152在体外可促进细胞增殖,在体内可促进肿瘤生长。此外,基于微阵列的分析表明,LINC00152可通过顺式调控与EpCAM启动子结合,激活雷帕霉素的机制性靶点(mTOR)途径,Gal4-λN/BoxB报告系统证实了这一点。因此,LINC00152可能通过激活mTOR信号通路参与肝癌的发生,未来可能成为临床诊断的新指标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4183/4767473/0127fd2802ba/oncotarget-06-42813-g001.jpg

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