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Biochem Biophys Res Commun. 2012 Aug 31;425(3):662-7. doi: 10.1016/j.bbrc.2012.07.114. Epub 2012 Jul 28.

Induction of the cellular microRNA-29c by influenza virus contributes to virus-mediated apoptosis through repression of antiapoptotic factors BCL2L2.

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  • 1Key Laboratory of Zoonosis, Ministry of Education, Institute of Zoonosis, Jilin University, Changchun 130062, PR China.


Influenza A virus is a cytolytic virus that induces apoptosis in numerous cell types, which contributes to cellular and organ dysfunction. MicroRNAs (miRNAs) represent a family of small noncoding RNAs controlling tanslation and transcription of many genes. Recent studies have revealed that miR-29c is involved in a variety of biological processes, including apoptosis. However, its role in influenza A virus infection is not well understood. Here, we report that miR-29c is involved in apoptosis induced by influenza A virus infection. We found that several apoptosis-associated miRNAs were stimulated in influenza A virus-infected A549 cells by miRNA array analysis. Within those, miR-29c was significantly up-regulated. In silico target prediction analysis revealed complementarity of miR-29c to the 3'-untranslated region (UTR) of BCL2L2 mRNA. Targeting of BCL2L2 3' UTR by miR-29c was determined by luciferase assay. Functional overexpression of miR-29c with miR-29c precursor inhibited BCL2L2 protein expression. Transfection of miR-29c inhibitor abolished both suppression of BCL2L2 protein expression and A549 cells apoptosis induced by influenza A virus. Moreover, BCL2L2 overexpression rescued A549 cell death induced by influenza A virus infection. These findings indicate that miR-29c-mediated BCL2L2 suppression is involved in influenza virus-induced cell death in A549 cells.

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