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10.1111/1759-7714.12628 http://scihub22266oqcxt.onion/10.1111/1759-7714.12628 C5928358!5928358!29575809     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29575809&cmd=llinks): Failed to open stream: HTTP request failed! 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IL?37 inhibits invasion and metastasis in non?small cell lung cancer by suppressing the IL?6/STAT3 signaling pathway |pdf=|usr=}}{{29575809}} gab.com Text IL 37 inhibits invasion and metastasis in non small cell lung cancer by suppressing the IL 6/STAT3 signaling pathway JO: Thorac Cancer http://www.kidney.de/pget.php?&tw=1&pmid=29575809 #FOAvip Background: IL?37 has been identified as a fundamental inhibitor of inflammatory and immunity responses. It plays a crucial protective role in several cancers, but its anti?tumor activity and the potential regulatory mechanism of IL?37 in non?small cell lung cancer (NSCLC) is largely unclear. Methods: Enzyme?linked immunosorbent assay was used to detect plasma IL?37 expression in NSCLC patients and healthy controls. The NSCLC cell line A549 was cultured with recombinant human IL?37 or recombinant human IL?6 protein. A549 invasion and metastasis were detected using Transwell invasion and scratch wound healing assays, respectively. Protein expression of STAT3, pSTAT3, E?cadherin, vimentin, and N?cadherin were detected using Western blotting, and messenger RNA expression of STAT3, E?cadherin, vimentin, and N?cadherin was assessed in each group using real time PCR. Results: IL?37 plasma expression was decreased in NSCLC patients, and the downregulation of IL?37 was correlated with tumor stage. In vitro, IL?37 inhibited invasion and migration in A549 cells, while IL?6 promoted invasion and migration in A549 cells. pSTAT3, vimentin, and N?cadherin expression was increased. E?cadherin expression was lower in the IL?6 group than in the control group; however, the opposite pattern was observed in the IL?37?+?IL?6 group. Conclusion: Our results showed that IL?37 plays an inhibitory role in NSCLC progression, possibly by suppressing STAT3 activation and decreasing epithelial?to?mesenchymal transition by inhibiting IL?6 expression. IL?37 could serve as a potential novel tumor suppressor in NSCLC. Twit Text FOAVip IL 37 inhibits invasion and metastasis in non small cell lung cancer by suppressing the IL 6/STAT3 signaling pathway ????Thorac Cancer http://www.kidney.de/pget.php?&tw=1&pmid=29575809 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29575809 #FOAvip English Wikipedia <ref>{{Cite pmid|29575809}}</ref> IL?37 inhibits invasion and metastasis in non?small cell lung cancer by suppressing the IL?6/STAT3 signaling pathway #MMPMID29575809 Jiang M; Wang Y; Zhang H; Ji Y; Zhao P; Sun R; Zhang C Thorac Cancer 2018[May]; 9 (5): 621-9 PMID29575809show ga Background: IL?37 has been identified as a fundamental inhibitor of inflammatory and immunity responses. It plays a crucial protective role in several cancers, but its anti?tumor activity and the potential regulatory mechanism of IL?37 in non?small cell lung cancer (NSCLC) is largely unclear. Methods: Enzyme?linked immunosorbent assay was used to detect plasma IL?37 expression in NSCLC patients and healthy controls. The NSCLC cell line A549 was cultured with recombinant human IL?37 or recombinant human IL?6 protein. A549 invasion and metastasis were detected using Transwell invasion and scratch wound healing assays, respectively. Protein expression of STAT3, pSTAT3, E?cadherin, vimentin, and N?cadherin were detected using Western blotting, and messenger RNA expression of STAT3, E?cadherin, vimentin, and N?cadherin was assessed in each group using real time PCR. Results: IL?37 plasma expression was decreased in NSCLC patients, and the downregulation of IL?37 was correlated with tumor stage. In vitro, IL?37 inhibited invasion and migration in A549 cells, while IL?6 promoted invasion and migration in A549 cells. pSTAT3, vimentin, and N?cadherin expression was increased. E?cadherin expression was lower in the IL?6 group than in the control group; however, the opposite pattern was observed in the IL?37?+?IL?6 group. Conclusion: Our results showed that IL?37 plays an inhibitory role in NSCLC progression, possibly by suppressing STAT3 activation and decreasing epithelial?to?mesenchymal transition by inhibiting IL?6 expression. IL?37 could serve as a potential novel tumor suppressor in NSCLC. �IL?37 inhibits invasion and metastasis in non?small cell lung cancer b(epmc).pdf DeepDyve Pubget Overpricing