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MicroRNA‐657 promotes tumorigenesis in hepatocellular carcinoma by targeting transducin‐like enhancer protein 1 through nuclear factor kappa B pathways
Author(s) -
Zhang Lisheng,
Yang Lixin,
Liu Xiyong,
Chen Wei,
Chang Lufen,
Chen Linling,
Loera Sofia,
Chu Peiguo,
Huang WeiChien,
Liu YunRu,
Yen Yun
Publication year - 2013
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.26162
Subject(s) - carcinogenesis , microrna , biology , cancer research , enhancer , hepatocellular carcinoma , hbx , signal transduction , cancer , microbiology and biotechnology , hepatitis b virus , gene expression , immunology , genetics , gene , virus
Growing evidence indicates that deregulation of microRNAs (miRNAs) contributes to tumorigenesis. Dysregulation of miR‐657 has been observed in several types of cancers, but its biological function is still largely unknown. Our results showed that miR‐657 expression can be induced by hepatitis viral proteins and is significantly increased in hepatocellular carcinoma (HCC) tissues. Moreover, introduction of miR‐657 dramatically increases proliferation and colony formation of HCC cells in vitro and induces tumor development in immunodeficient mice. Further studies showed that miR‐657 directly targets the transducin‐like enhancer protein 1 (TLE1) 3′ untranslated region (UTR) and activates nuclear factor kappa B (NF‐κB) pathways that contribute to hepatocarcinogenesis. Conclusion : This study identified a mechanism whereby miRNA‐657 contributed to HCC through novel cancer pathways and provides new insights into the potential molecular mechanisms of hepatic carcinogenesis. (H EPATOLOGY 2013)