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10.7150/ijbs.13475 http://scihub22266oqcxt.onion/10.7150/ijbs.13475 C4807160!4807160 !27019625     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27019625 &cmd=llinks): Failed to open stream: HTTP request failed! 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MiR-487a Promotes TGF-?1-induced EMT, the Migration and Invasion of Breast Cancer Cells by Directly Targeting MAGI2 |pdf=|usr=}}{{27019625 }} gab.com Text MiR-487a Promotes TGF- 1-induced EMT, the Migration and Invasion of Breast Cancer Cells by Directly Targeting MAGI2 JO: Int J Biol Sci http://www.kidney.de/pget.php?&tw=1&pmid=27019625 #FOAvip Tumor metastasis is a complex and multistep process and its exact molecular mechanisms remain unclear. We attempted to find novel microRNAs (miRNAs) contributing to the migration and invasion of breast cancer cells. In this study, we found that the expression of miR-487a was higher in MDA-MB-231breast cancer cells with high metastasis ability than MCF-7 breast cancer cells with low metastasis ability and the treatment with transforming growth factor ?1 (TGF-?1) significantly increased the expression of miR-487a in MCF-7 and MDA-MB-231 breast cancer cells. Subsequently, we found that the transfection of miR-487a inhibitor significantly decreased the expression of vimentin, a mesenchymal marker, while increased the expression of E-cadherin, an epithelial marker, in both MCF-7 cells and MDA-MB-231 cells. Also, the inactivation of miR-487a inhibited the migration and invasion of breast cancer cells. Furthermore, our findings demonstrated that miR-487a directly targeted the MAGI2 involved in the stability of PTEN. The down-regulation of miR-487a increased the expression of p-PTEN and PTEN, and reduced the expression of p-AKT in both cell lines. In addition, the results showed that NF-kappaB (p65) significantly increased the miR-487a promoter activity and expression, and TGF-?1 induced the increased miR-487a promoter activity via p65 in MCF-7 cells and MDA-MB-231 cells. Moreover, we further confirmed the expression of miR-487a was positively correlated with the lymph nodes metastasis and negatively correlated with the expression of MAGI2 in human breast cancer tissues. Overall, our results suggested that miR-487a could promote the TGF-?1-induced EMT, the migration and invasion of breast cancer cells by directly targeting MAGI2. Twit Text FOAVip MiR-487a Promotes TGF- 1-induced EMT, the Migration and Invasion of Breast Cancer Cells by Directly Targeting MAGI2 ????Int J Biol Sci http://www.kidney.de/pget.php?&tw=1&pmid=27019625 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27019625 #FOAvip English Wikipedia <ref>{{Cite pmid|27019625 }}</ref> MiR-487a Promotes TGF-?1-induced EMT, the Migration and Invasion of Breast Cancer Cells by Directly Targeting MAGI2 #MMPMID27019625 Ma M ; He M ; Jiang Q ; Yan Y ; Guan S ; Zhang J ; Yu Z ; Chen Q ; Sun M ; Yao W ; Zhao H ; Jin F ; Wei M Int J Biol Sci 2016[]; 12 (4 ): 397-408 PMID27019625 show ga Tumor metastasis is a complex and multistep process and its exact molecular mechanisms remain unclear. We attempted to find novel microRNAs (miRNAs) contributing to the migration and invasion of breast cancer cells. In this study, we found that the expression of miR-487a was higher in MDA-MB-231breast cancer cells with high metastasis ability than MCF-7 breast cancer cells with low metastasis ability and the treatment with transforming growth factor ?1 (TGF-?1) significantly increased the expression of miR-487a in MCF-7 and MDA-MB-231 breast cancer cells. Subsequently, we found that the transfection of miR-487a inhibitor significantly decreased the expression of vimentin, a mesenchymal marker, while increased the expression of E-cadherin, an epithelial marker, in both MCF-7 cells and MDA-MB-231 cells. Also, the inactivation of miR-487a inhibited the migration and invasion of breast cancer cells. Furthermore, our findings demonstrated that miR-487a directly targeted the MAGI2 involved in the stability of PTEN. The down-regulation of miR-487a increased the expression of p-PTEN and PTEN, and reduced the expression of p-AKT in both cell lines. In addition, the results showed that NF-kappaB (p65) significantly increased the miR-487a promoter activity and expression, and TGF-?1 induced the increased miR-487a promoter activity via p65 in MCF-7 cells and MDA-MB-231 cells. Moreover, we further confirmed the expression of miR-487a was positively correlated with the lymph nodes metastasis and negatively correlated with the expression of MAGI2 in human breast cancer tissues. Overall, our results suggested that miR-487a could promote the TGF-?1-induced EMT, the migration and invasion of breast cancer cells by directly targeting MAGI2. |Adaptor Proteins, Signal Transducing [MESH] |Carrier Proteins/genetics/*metabolism [MESH] |Cell Line, Tumor [MESH] |Epithelial-Mesenchymal Transition/*drug effects/genetics [MESH] |Gene Expression Regulation, Neoplastic/genetics/physiology [MESH] |Guanylate Kinases [MESH] |HEK293 Cells [MESH] |Humans [MESH] |MCF-7 Cells [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Neoplasm Invasiveness/genetics/physiopathology [MESH]MiR-487a Promotes TGF-?1-induced EMT, the Migration and Invasion of Br(epmc).pdf DeepDyve Pubget Overpricing