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10.3892/or.2018.6424 http://scihub22266oqcxt.onion/10.3892/or.2018.6424 C6059753!6059753!29749532     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncol+Rep 2018 ; 40 (1): 39-48 Nephropedia Template TP {{tp|p=29749532|t=2018. MEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesenchymal transition in gastric cancer |pdf=|usr=}}{{29749532}} gab.com Text MEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesenchymal transition in gastric cancer JO: Oncol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29749532 #FOAvip The prognosis of patients with gastric cancer remains poor mainly due to distant metastasis. Maternally expressed gene 3 (MEG3), a long non-coding RNA (lncRNA), is downregulated in various tumor tissues and suppresses tumor progression. miR-21 is a microRNA which is expressed highly in tumor tissues. In the present study, we investigated the relationship between MEG3 and miR-21 in regards to the cell mobility of gastric cancer. Our data demonstrated that MEG3 was downregulated while miR-21 was upregulated in gastric cancer tissues and cell lines by qRT-PCR. Overexpression of MEG3 suppressed cell mobility of gastric cancer cells (AGS) by downregulating the expression of MMP-3, MMP-9 and VEGF. As shown by western blot analysis, overexpression of MEG3 also suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of an epithelial marker (E-cadherin) and downregulating the expression of mesenchymal markers (N-cadherin, Snail and ?-catenin), indicating that MEG3 suppressed cell mobility through the inhibition of EMT in gastric cancer. The expression of miR-21 was negatively regulated by MEG3 and overexpression of miR-21 promoted cell mobility of AGS through activation of EMT. Co-transfection of lncRNA-MEG3 and miR-21 mimic counteracted the inhibitory effect on the cell mobility attributed to MEG3, suggesting that the MEG3/miR-21 axis affects cell mobility by suppressing EMT in gastric cancer. Using a mouse xenograft tumor model, we found that the overexpression of MEG3 suppressed tumor growth and metastasis while overexpression of miR-21 had the opposite effects. The MEG3/miR-21 axis affected gastric cancer growth and metastasis through inhibition of EMT in vivo. In conclusion, we demonstrated that the MEG3/miR-21 axis participates in the tumor progression and metastasis of gastric cancer through the regulation of EMT. Twit Text FOAVip MEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesenchymal transition in gastric cancer ????Oncol Rep http://www.kidney.de/pget.php?&tw=1&pmid=29749532 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29749532 #FOAvip English Wikipedia <ref>{{Cite pmid|29749532}}</ref> MEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesenchymal transition in gastric cancer #MMPMID29749532 Xu G; Meng L; Yuan D; Li K; Zhang Y; Dang C; Zhu K Oncol Rep 2018[Jul]; 40 (1): 39-48 PMID29749532show ga The prognosis of patients with gastric cancer remains poor mainly due to distant metastasis. Maternally expressed gene 3 (MEG3), a long non-coding RNA (lncRNA), is downregulated in various tumor tissues and suppresses tumor progression. miR-21 is a microRNA which is expressed highly in tumor tissues. In the present study, we investigated the relationship between MEG3 and miR-21 in regards to the cell mobility of gastric cancer. Our data demonstrated that MEG3 was downregulated while miR-21 was upregulated in gastric cancer tissues and cell lines by qRT-PCR. Overexpression of MEG3 suppressed cell mobility of gastric cancer cells (AGS) by downregulating the expression of MMP-3, MMP-9 and VEGF. As shown by western blot analysis, overexpression of MEG3 also suppressed epithelial-mesenchymal transition (EMT) by increasing the expression of an epithelial marker (E-cadherin) and downregulating the expression of mesenchymal markers (N-cadherin, Snail and ?-catenin), indicating that MEG3 suppressed cell mobility through the inhibition of EMT in gastric cancer. The expression of miR-21 was negatively regulated by MEG3 and overexpression of miR-21 promoted cell mobility of AGS through activation of EMT. Co-transfection of lncRNA-MEG3 and miR-21 mimic counteracted the inhibitory effect on the cell mobility attributed to MEG3, suggesting that the MEG3/miR-21 axis affects cell mobility by suppressing EMT in gastric cancer. Using a mouse xenograft tumor model, we found that the overexpression of MEG3 suppressed tumor growth and metastasis while overexpression of miR-21 had the opposite effects. The MEG3/miR-21 axis affected gastric cancer growth and metastasis through inhibition of EMT in vivo. In conclusion, we demonstrated that the MEG3/miR-21 axis participates in the tumor progression and metastasis of gastric cancer through the regulation of EMT. äMEG3/miR-21 axis affects cell mobility by suppressing epithelial-mesen(epmc).pdf DeepDyve Pubget Overpricing