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10.1038/onc.2014.203 http://scihub22266oqcxt.onion/10.1038/onc.2014.203 C4761647!4761647!25023698     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25023698&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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncogene 2015 ; 34 (20): 2597-608 Nephropedia Template TP {{tp|p=25023698|t=2015. Dual inhibition of REV-ERB? and autophagy as a novel pharmacological approach to induce cytotoxicity in cancer cells |pdf=|usr=}}{{25023698}} gab.com Text Dual inhibition of REV-ERB and autophagy as a novel pharmacological approach to induce cytotoxicity in cancer cells JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=25023698 #FOAvip REV-ERB? and REV-ERB? nuclear receptors regulate several physiological processes, including circadian rhythm and metabolism. A previous study reported the REV-ERB? gene to be co-overexpressed with ERBB2 in breast cancer cell lines. Surprisingly, we found that several tumor types, including a number of breast cancer cell lines, predominantly express the REV-ERB? variant. This pattern was independent of ERBB2 and ER status, and opposite to that of non-cancer mammary epithelial HMEC cells, in which REV-ERB? was the major variant. Consistent with this molecular profile, REV-ERB target genes in both circadian and metabolic pathways were derepressed upon silencing of REV-ERB?, but not REV-ERB?. Strikingly, we found that REV-ERB? is a determinant of sensitivity to chloroquine, a clinically relevant lysosomotropic agent that suppresses autophagy. The cytoprotective function of REV-ERB? appears to operate downstream of autophagy blockade. Through compound screening, we identified ARN5187, a novel lysosomotropic REV-ERB? ligand with a dual inhibitory activity toward REV-ERB-mediated transcriptional regulation and autophagy. Remarkably, although ARN5187 and chloroquine share similar lysosomotropic potency and have a similar effect on autophagy inhibition, ARN5187 is significantly more cytotoxic. Collectively, our results reveal that dual inhibition of REV-ERB? and autophagy is an effective strategy for eliciting cytotoxicity in cancer cells. Furthermore, our discovery of a novel inhibitor compound of both REV-ERB and autophagy may provide a scaffold for the discovery of new multifunctional anticancer agents. Twit Text FOAVip Dual inhibition of REV-ERB and autophagy as a novel pharmacological approach to induce cytotoxicity in cancer cells ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=25023698 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25023698 #FOAvip English Wikipedia <ref>{{Cite pmid|25023698}}</ref> Dual inhibition of REV-ERB? and autophagy as a novel pharmacological approach to induce cytotoxicity in cancer cells #MMPMID25023698 De Mei C; Ercolani L; Parodi C; Veronesi M; Vecchio CL; Bottegoni G; Torrente E; Scarpelli R; Marotta R; Ruffili R; Mattioli M; Reggiani A; Wade M; Grimaldi B Oncogene 2015[May]; 34 (20): 2597-608 PMID25023698show ga REV-ERB? and REV-ERB? nuclear receptors regulate several physiological processes, including circadian rhythm and metabolism. A previous study reported the REV-ERB? gene to be co-overexpressed with ERBB2 in breast cancer cell lines. Surprisingly, we found that several tumor types, including a number of breast cancer cell lines, predominantly express the REV-ERB? variant. This pattern was independent of ERBB2 and ER status, and opposite to that of non-cancer mammary epithelial HMEC cells, in which REV-ERB? was the major variant. Consistent with this molecular profile, REV-ERB target genes in both circadian and metabolic pathways were derepressed upon silencing of REV-ERB?, but not REV-ERB?. Strikingly, we found that REV-ERB? is a determinant of sensitivity to chloroquine, a clinically relevant lysosomotropic agent that suppresses autophagy. The cytoprotective function of REV-ERB? appears to operate downstream of autophagy blockade. Through compound screening, we identified ARN5187, a novel lysosomotropic REV-ERB? ligand with a dual inhibitory activity toward REV-ERB-mediated transcriptional regulation and autophagy. Remarkably, although ARN5187 and chloroquine share similar lysosomotropic potency and have a similar effect on autophagy inhibition, ARN5187 is significantly more cytotoxic. Collectively, our results reveal that dual inhibition of REV-ERB? and autophagy is an effective strategy for eliciting cytotoxicity in cancer cells. Furthermore, our discovery of a novel inhibitor compound of both REV-ERB and autophagy may provide a scaffold for the discovery of new multifunctional anticancer agents. äDual inhibition of REV-ERB? and autophagy as a novel pharmacological a(epmc).pdf DeepDyve Pubget Overpricing