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10.18632/oncotarget.13137 http://scihub22266oqcxt.onion/10.18632/oncotarget.13137 C5349884!5349884 !27829234     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27829234 &cmd=llinks): Failed to open stream: HTTP request failed! 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A regulatory loop involving miR-29c and Sp1 elevates the TGF-?1 mediated epithelial-to-mesenchymal transition in lung cancer |pdf=|usr=}}{{27829234 }} gab.com Text A regulatory loop involving miR-29c and Sp1 elevates the TGF- 1 mediated epithelial-to-mesenchymal transition in lung cancer JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27829234 #FOAvip Specificity protein1 (Sp1) is required for TGF-?-induced epithelial-to-mesenchymal transition (EMT) which has been demonstrated to aggravate the progression of cancer including lung cancer. microRNA-29c (miR-29c) is identified to inhibit EMT, but the correlation between miR-29c and Sp1 in human lung cancer remain incompletely clarified. Here, we confirmed decreased expression of miR-29c and enhanced expression of Sp1 in lung cancer tissues (n = 20) and found that Sp1 could be targeted and inhibited by miR-29c. Besides, the expression of miR-29c was down-regulated in high-metastatic lung cancer cell lines and TGF-?1-treated cells. The inhibition of miR-29c or overexpression of Sp1 in 95C and A549 cells dramatically enhanced the cell migration and invasion, and also induced the decrease in the expression of epithelial markers, e.g. thyroid transcription factor 1 (TTF-1) and E-cadherin, together with an increase in mesenchymal markers including vimentin, ?-smooth muscle actin (?-SMA), which could be restored by overexpression of miR-29c mimics during the TGF-?-induced EMT. Moreover, dual-luciferase reporter assay was performed and the results indicated that miR-29c/Sp1 could form an auto-regulatory loop with TGF-?1, which impaired TGFB1 transcription. Furthermore, miR-29c overexpression could abrogate the tumor progression and inhibit the Sp1/TGF-? expressions in vivo, indicating that miR-29c could be a tumor suppressor and repress the Sp1/TGF-? axis-induced EMT in lung cancer. Twit Text FOAVip A regulatory loop involving miR-29c and Sp1 elevates the TGF- 1 mediated epithelial-to-mesenchymal transition in lung cancer ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27829234 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27829234 #FOAvip English Wikipedia <ref>{{Cite pmid|27829234 }}</ref> A regulatory loop involving miR-29c and Sp1 elevates the TGF-?1 mediated epithelial-to-mesenchymal transition in lung cancer #MMPMID27829234 Zhang HW ; Wang EW ; Li LX ; Yi SH ; Li LC ; Xu FL ; Wang DL ; Wu YZ ; Nian WQ Oncotarget 2016[Dec]; 7 (52 ): 85905-85916 PMID27829234 show ga Specificity protein1 (Sp1) is required for TGF-?-induced epithelial-to-mesenchymal transition (EMT) which has been demonstrated to aggravate the progression of cancer including lung cancer. microRNA-29c (miR-29c) is identified to inhibit EMT, but the correlation between miR-29c and Sp1 in human lung cancer remain incompletely clarified. Here, we confirmed decreased expression of miR-29c and enhanced expression of Sp1 in lung cancer tissues (n = 20) and found that Sp1 could be targeted and inhibited by miR-29c. Besides, the expression of miR-29c was down-regulated in high-metastatic lung cancer cell lines and TGF-?1-treated cells. The inhibition of miR-29c or overexpression of Sp1 in 95C and A549 cells dramatically enhanced the cell migration and invasion, and also induced the decrease in the expression of epithelial markers, e.g. thyroid transcription factor 1 (TTF-1) and E-cadherin, together with an increase in mesenchymal markers including vimentin, ?-smooth muscle actin (?-SMA), which could be restored by overexpression of miR-29c mimics during the TGF-?-induced EMT. Moreover, dual-luciferase reporter assay was performed and the results indicated that miR-29c/Sp1 could form an auto-regulatory loop with TGF-?1, which impaired TGFB1 transcription. Furthermore, miR-29c overexpression could abrogate the tumor progression and inhibit the Sp1/TGF-? expressions in vivo, indicating that miR-29c could be a tumor suppressor and repress the Sp1/TGF-? axis-induced EMT in lung cancer. |Animals [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Epithelial-Mesenchymal Transition [MESH] |Humans [MESH] |Lung Neoplasms/*pathology [MESH] |Mice [MESH] |MicroRNAs/*physiology [MESH] |Neoplasm Invasiveness [MESH] |Sp1 Transcription Factor/*physiology [MESH]A regulatory loop involving miR-29c and Sp1 elevates the TGF-?1 mediat(epmc).pdf DeepDyve Pubget Overpricing