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10.1158/1078-0432.CCR-13-2658 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-13-2658 C4269153!4269153 !24727327     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24727327 &cmd=llinks): Failed to open stream: HTTP request failed! 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Small-molecule RA-9 inhibits proteasome-associated DUBs and ovarian cancer in vitro and in vivo via exacerbating unfolded protein responses |pdf=|usr=}}{{24727327 }} gab.com Text Small-molecule RA-9 inhibits proteasome-associated DUBs and ovarian cancer in vitro and in vivo via exacerbating unfolded protein responses JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24727327 #FOAvip PURPOSE: Ovarian cancer is the deadliest of the gynecologic malignancies. Carcinogenic progression is accompanied by upregulation of ubiquitin-dependent protein degradation machinery as a mechanism to compensate with elevated endogenous proteotoxic stress. Recent studies support the notion that deubiquitinating enzymes (DUB) are essential factors in proteolytic degradation and that their aberrant activity is linked to cancer progression and chemoresistance. Thus, DUBs are an attractive therapeutic target for ovarian cancer. EXPERIMENTAL DESIGN: The potency and selectivity of RA-9 inhibitor for proteasome-associated DUBs was determined in ovarian cancer cell lines and primary cells. The anticancer activity of RA-9 and its mechanism of action were evaluated in multiple cancer cell lines in vitro and in vivo in immunodeficient mice bearing an intraperitoneal ES-2 xenograft model of human ovarian cancer. RESULTS: Here, we report the characterization of RA-9 as a small-molecule inhibitor of proteasome-associated DUBs. Treatment with RA-9 selectively induces onset of apoptosis in ovarian cancer cell lines and primary cultures derived from donors. Loss of cell viability following RA-9 exposure is associated with an unfolded protein response as mechanism to compensate for unsustainable levels of proteotoxic stress. In vivo treatment with RA-9 retards tumor growth, increases overall survival, and was well tolerated by the host. CONCLUSIONS: Our preclinical studies support further evaluation of RA-9 as an ovarian cancer therapeutic. Twit Text FOAVip Small-molecule RA-9 inhibits proteasome-associated DUBs and ovarian cancer in vitro and in vivo via exacerbating unfolded protein responses ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24727327 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24727327 #FOAvip English Wikipedia <ref>{{Cite pmid|24727327 }}</ref> Small-molecule RA-9 inhibits proteasome-associated DUBs and ovarian cancer in vitro and in vivo via exacerbating unfolded protein responses #MMPMID24727327 Coughlin K ; Anchoori R ; Iizuka Y ; Meints J ; MacNeill L ; Vogel RI ; Orlowski RZ ; Lee MK ; Roden RB ; Bazzaro M Clin Cancer Res 2014[Jun]; 20 (12 ): 3174-86 PMID24727327 show ga PURPOSE: Ovarian cancer is the deadliest of the gynecologic malignancies. Carcinogenic progression is accompanied by upregulation of ubiquitin-dependent protein degradation machinery as a mechanism to compensate with elevated endogenous proteotoxic stress. Recent studies support the notion that deubiquitinating enzymes (DUB) are essential factors in proteolytic degradation and that their aberrant activity is linked to cancer progression and chemoresistance. Thus, DUBs are an attractive therapeutic target for ovarian cancer. EXPERIMENTAL DESIGN: The potency and selectivity of RA-9 inhibitor for proteasome-associated DUBs was determined in ovarian cancer cell lines and primary cells. The anticancer activity of RA-9 and its mechanism of action were evaluated in multiple cancer cell lines in vitro and in vivo in immunodeficient mice bearing an intraperitoneal ES-2 xenograft model of human ovarian cancer. RESULTS: Here, we report the characterization of RA-9 as a small-molecule inhibitor of proteasome-associated DUBs. Treatment with RA-9 selectively induces onset of apoptosis in ovarian cancer cell lines and primary cultures derived from donors. Loss of cell viability following RA-9 exposure is associated with an unfolded protein response as mechanism to compensate for unsustainable levels of proteotoxic stress. In vivo treatment with RA-9 retards tumor growth, increases overall survival, and was well tolerated by the host. CONCLUSIONS: Our preclinical studies support further evaluation of RA-9 as an ovarian cancer therapeutic. |Animals [MESH] |Apoptosis/drug effects [MESH] |Benzylidene Compounds/*pharmacology [MESH] |Blotting, Western [MESH] |Cell Cycle/drug effects [MESH] |Cell Proliferation/drug effects [MESH] |Female [MESH] |Flow Cytometry [MESH] |Humans [MESH] |Immunoenzyme Techniques [MESH] |In Vitro Techniques [MESH] |Mice [MESH] |Mice, Nude [MESH] |Ovarian Neoplasms/*drug therapy/enzymology/pathology [MESH] |Piperidones/*pharmacology [MESH] |Proteasome Endopeptidase Complex/*chemistry [MESH] |Proteasome Inhibitors/*pharmacology [MESH] |Small Molecule Libraries/*pharmacology [MESH] |Tumor Cells, Cultured [MESH] |Ubiquitin-Specific Proteases/*antagonists & inhibitors [MESH] |Ubiquitin/metabolism [MESH] |Unfolded Protein Response/*drug effects [MESH]Small-molecule RA-9 inhibits proteasome-associated DUBs and ovarian ca(epmc).pdf DeepDyve Pubget Overpricing