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10.4196/kjpp.2016.20.2.161 http://scihub22266oqcxt.onion/10.4196/kjpp.2016.20.2.161 C4770106!4770106 !26937212     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26937212 &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       Korean+J+Physiol+Pharmacol 2016 ; 20 (2 ): 161-8 Nephropedia Template TP {{tp|p=26937212 |t=2016. CRM1 inhibitor S109 suppresses cell proliferation and induces cell cycle arrest in renal cancer cells |pdf=|usr=}}{{26937212 }} gab.com Text CRM1 inhibitor S109 suppresses cell proliferation and induces cell cycle arrest in renal cancer cells JO: Korean J Physiol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=26937212 #FOAvip Abnormal localization of tumor suppressor proteins is a common feature of renal cancer. Nuclear export of these tumor suppressor proteins is mediated by chromosome region maintenance-1 (CRM1). Here, we investigated the antitumor eff ects of a novel reversible inhibitor of CRM1 on renal cancer cells. We found that S109 inhibits the CRM1-mediated nuclear export of RanBP1 and reduces protein levels of CRM1. Furthermore, the inhibitory eff ect of S109 on CRM1 is reversible. Our data demonstrated that S109 signifi cantly inhibits proliferation and colony formation of renal cancer cells. Cell cycle assay showed that S109 induced G1-phase arrest, followed by the reduction of Cyclin D1 and increased expression of p53 and p21. We also found that S109 induces nuclear accumulation of tumor suppressor proteins, Foxo1 and p27. Most importantly, mutation of CRM1 at Cys528 position abolished the eff ects of S109. Taken together, our results indicate that CRM1 is a therapeutic target in renal cancer and the novel reversible CRM1 inhibitor S109 can act as a promising candidate for renal cancer therapy. Twit Text FOAVip CRM1 inhibitor S109 suppresses cell proliferation and induces cell cycle arrest in renal cancer cells ????Korean J Physiol Pharmacol http://www.kidney.de/pget.php?&tw=1&pmid=26937212 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26937212 #FOAvip English Wikipedia <ref>{{Cite pmid|26937212 }}</ref> CRM1 inhibitor S109 suppresses cell proliferation and induces cell cycle arrest in renal cancer cells #MMPMID26937212 Liu X ; Chong Y ; Liu H ; Han Y ; Niu M Korean J Physiol Pharmacol 2016[Mar]; 20 (2 ): 161-8 PMID26937212 show ga Abnormal localization of tumor suppressor proteins is a common feature of renal cancer. Nuclear export of these tumor suppressor proteins is mediated by chromosome region maintenance-1 (CRM1). Here, we investigated the antitumor eff ects of a novel reversible inhibitor of CRM1 on renal cancer cells. We found that S109 inhibits the CRM1-mediated nuclear export of RanBP1 and reduces protein levels of CRM1. Furthermore, the inhibitory eff ect of S109 on CRM1 is reversible. Our data demonstrated that S109 signifi cantly inhibits proliferation and colony formation of renal cancer cells. Cell cycle assay showed that S109 induced G1-phase arrest, followed by the reduction of Cyclin D1 and increased expression of p53 and p21. We also found that S109 induces nuclear accumulation of tumor suppressor proteins, Foxo1 and p27. Most importantly, mutation of CRM1 at Cys528 position abolished the eff ects of S109. Taken together, our results indicate that CRM1 is a therapeutic target in renal cancer and the novel reversible CRM1 inhibitor S109 can act as a promising candidate for renal cancer therapy. ?CRM1 inhibitor S109 suppresses cell proliferation and induces cell cyc(epmc).pdf DeepDyve Pubget Overpricing