miR-16 promotes the apoptosis of human cancer cells by targeting FEAT

miR-16 promotes the apoptosis of human cancer cells by targeting FEAT
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DOI：
10.1186/s12885-015-1458-8
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发表时间：
2015
期刊：
BMC Cancer
影响因子：
--
通讯作者：
Guangxin Zhou
Guangxin Zhou
中科院分区：
--
文献类型：
--
作者：
Hongwei Liang;Zheng Fu;Xueyuan Jiang;Nan Wang;FengWang;Xueliang Wang;Suyang Zhang;Yanbo Wang;Xin Yan;Wen-xian Guan;Chen-Yu Zhang;Ke Zen;Yujing Zhang;Xi Chen;Guangxin Zhou

文献摘要

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Background: Although human cancers have heterogeneous combinations of altered oncogenes, some crucial.genes are universally dysregulated in most cancers. One such gene, FEAT (faint expression in normal tissues,.aberrant overexpression in tumors), is uniformly overexpressed in a variety of human cancers and plays an.important role in tumorigenesis by suppressing apoptosis. However, the precise molecular mechanism through.which FEAT is upregulated during tumorigenesis remains largely unknown..Methods: In this study, we used bioinformatic analyses to search for miRNAs that potentially target FEAT. We examined.the expression of FEAT protein level by western blotting and miR-16 level by qRT-PCR assay. Cancer cell lines (A549, MCF-7.and Huh-7) with miR-16 upregulation and FEAT silencing were established and the effects on apoptosis of cancer cells.in vitro were assessed. Luciferase reporter assay was also performed to investigate the interaction between miR-16 and FEAT..Results: We identified a specific target site for miR-16 in the 3′-untranslated region (3′-UTR) of FEAT. Consistent with.the bioinformatic analyses, we identified an inverse correlation between the miR-16 and FEAT protein levels in.lung cancer, breast cancer, and hepatocellular cancer tissues. We then experimentally validated miR-16 as a direct.regulator of FEAT using cell transfection and luciferase assays. Finally, we demonstrated that the repression of FEAT.by miR-16 promoted the apoptosis of cancer cells..Conclusions: Our findings provide the first clues regarding the role of miR-16 as a tumor suppressor in cancer cells.through the inhibition of FEAT translation.