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10.21037/tcr-20-1006 http://scihub22266oqcxt.onion/10.21037/tcr-20-1006 35117228!8798353!35117228     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=35117228&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Transl+Cancer+Res 2020 ; 9 (10): 6178-6188 Nephropedia Template TP {{tp|p=35117228|t=2020. MEST promotes bladder cancer cell proliferation, migration and invasion via STAT3/Twist-1-mediated EMT |pdf=|usr=}}{{35117228}} gab.com Text MEST promotes bladder cancer cell proliferation, migration and invasion via STAT3/Twist-1-mediated EMT JO: Transl Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=35117228 #FOAvip BACKGROUND: Mesoderm-specific transcript (MEST) has been demonstrated to be a proto-oncogene or anti-oncogene in various carcinomas. However, the role and mechanism of MEST in bladder cancer (BC) are still unknown. Here we aimed to explore the effect of MEST on malignant biological behaviour in BC and its potential mechanism. METHODS: The expression of MEST in BC tissues and cells was detected by qRT-PCR methods. MEST depletion and overexpression cell lines were established in T24 and 5637 respectively. Then the effects of MEST on cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) were investigated. Finally, the STAT3/Twist-1 signaling was verified. RESULTS: MEST was elevated in BC tissues and cells lines, and its high expression was highly relevant to the clinicopathologic features of patients with BC and to poor prognosis in these patients. MEST depletion impeded cell proliferation, migration and invasion as well as epithelial-mesenchymal transition (EMT), while MEST overexpression promoted malignant biological behaviour in BC. Mechanistically, MEST upregulated p-STAT3 and Twist-1 expression, while treatment with a STAT3 inhibitor clearly attenuated the STAT3 activation and Twist-1 upregulation induced by MEST. Subsequently, rescue assays confirmed that inhibition of STAT3 signalling could remarkably relieve the oncogenic effects of MEST on malignant biological behaviour in BC. CONCLUSIONS: Our data confirmed that MEST exerts oncogenic functions in bladder cancer via STAT3/Twist-1 signalling and that MEST may represent a promising target in BC treatment. Twit Text FOAVip MEST promotes bladder cancer cell proliferation, migration and invasion via STAT3/Twist-1-mediated EMT ????Transl Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=35117228 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35117228 #FOAvip English Wikipedia <ref>{{Cite pmid|35117228}}</ref> MEST promotes bladder cancer cell proliferation, migration and invasion via STAT3/Twist-1-mediated EMT #MMPMID35117228 Zhao C; Hu X; Tong S; Mo M; He W; Wang L; Li Y Transl Cancer Res 2020[Oct]; 9 (10): 6178-6188 PMID35117228show ga BACKGROUND: Mesoderm-specific transcript (MEST) has been demonstrated to be a proto-oncogene or anti-oncogene in various carcinomas. However, the role and mechanism of MEST in bladder cancer (BC) are still unknown. Here we aimed to explore the effect of MEST on malignant biological behaviour in BC and its potential mechanism. METHODS: The expression of MEST in BC tissues and cells was detected by qRT-PCR methods. MEST depletion and overexpression cell lines were established in T24 and 5637 respectively. Then the effects of MEST on cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) were investigated. Finally, the STAT3/Twist-1 signaling was verified. RESULTS: MEST was elevated in BC tissues and cells lines, and its high expression was highly relevant to the clinicopathologic features of patients with BC and to poor prognosis in these patients. MEST depletion impeded cell proliferation, migration and invasion as well as epithelial-mesenchymal transition (EMT), while MEST overexpression promoted malignant biological behaviour in BC. Mechanistically, MEST upregulated p-STAT3 and Twist-1 expression, while treatment with a STAT3 inhibitor clearly attenuated the STAT3 activation and Twist-1 upregulation induced by MEST. Subsequently, rescue assays confirmed that inhibition of STAT3 signalling could remarkably relieve the oncogenic effects of MEST on malignant biological behaviour in BC. CONCLUSIONS: Our data confirmed that MEST exerts oncogenic functions in bladder cancer via STAT3/Twist-1 signalling and that MEST may represent a promising target in BC treatment. ?MEST promotes bladder cancer cell proliferation, migration and invasio(epmc).pdf DeepDyve Pubget Overpricing