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10.1186/s12885-015-1458-8 http://scihub22266oqcxt.onion/10.1186/s12885-015-1458-8 C4450989!4450989!26031775     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       BMC+Cancer 2015 ; 15 (ä): ä Nephropedia Template TP {{tp|p=26031775|t=2015. miR-16 promotes the apoptosis of human cancer cells by targeting FEAT |pdf=|usr=}}{{26031775}} gab.com Text miR-16 promotes the apoptosis of human cancer cells by targeting FEAT JO: BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26031775 #FOAvip 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. Electronic supplementary material: The online version of this article (doi:10.1186/s12885-015-1458-8) contains supplementary material, which is available to authorized users. Twit Text FOAVip miR-16 promotes the apoptosis of human cancer cells by targeting FEAT ????BMC Cancer http://www.kidney.de/pget.php?&tw=1&pmid=26031775 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26031775 #FOAvip English Wikipedia <ref>{{Cite pmid|26031775}}</ref> miR-16 promotes the apoptosis of human cancer cells by targeting FEAT #MMPMID26031775 Liang H; Fu Z; Jiang X; Wang N; Wang F; Wang X; Zhang S; Wang Y; Yan X; Guan Wx; Zhang CY; Zen K; Zhang Y; Chen X; Zhou G BMC Cancer 2015[]; 15 (ä): ä PMID26031775show ga 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. Electronic supplementary material: The online version of this article (doi:10.1186/s12885-015-1458-8) contains supplementary material, which is available to authorized users. ämiR-16 promotes the apoptosis of human cancer cells by targeting FEAT (epmc).pdf DeepDyve Pubget Overpricing