miR-122 targets an anti-apoptotic gene, Bcl-w, in human hepatocellular carcinoma cell lines

• Published in: Biochemical and biophysical research communications Vol. 375; no. 3; pp. 315 - 320
• Main Authors: Lin, Cliff Ji-Fan, Gong, Hong-Yi, Tseng, Hung-Chia, Wang, Wei-Lun, Wu, Jen-Leih
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 24.10.2008
• Subjects: 3' Untranslated Regions; Apoptosis; Apoptosis Regulatory Proteins - genetics; Apoptosis Regulatory Proteins - metabolism; Base Sequence; Bcl-w; Carcinoma, Hepatocellular - genetics; Carcinoma, Hepatocellular - metabolism; Caspase 3 - metabolism; Cell Survival; Down-Regulation; Enzyme Activation; Genetic Vectors; Hepatocellular carcinoma; Humans; Liver Neoplasms - genetics; Liver Neoplasms - metabolism; MicroRNAs - genetics; MicroRNAs - physiology; miR-122; Molecular Sequence Data; RNA, Small Interfering - genetics; Transfection; Bcl-w; Hepatocellular carcinoma; miR-122
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2008.07.154

miR-122, a hepato-specific microRNA (miRNA), is frequently down-regulated in human hepatocellular carcinoma (HCC). In an effort to identify novel miR-122 targets, we performed an in silico analysis and detected a putative binding site in the 3′-untranslated region (3′-UTR) of Bcl-w, an anti-apoptotic Bcl-2 family member. In the HCC-derived cell lines, Hep3B and HepG2, we confirmed that miR-122 modulates Bcl-w expression by directly targeting binding site within the 3′-UTR. The cellular mRNA and protein levels of Bcl-w were repressed by elevated levels of miR-122, which subsequently led to reduction of cell viability and activation of caspase-3. Thus, Bcl-w is a direct target of miR-122 that functions as an endogenous apoptosis regulator in these HCC-derived cell lines.