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10.1530/ERC-14-0402 http://scihub22266oqcxt.onion/10.1530/ERC-14-0402 C4233119!4233119!25287069     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Endocr+Relat+Cancer 2014 ; 21 (6): 903-14 Nephropedia Template TP {{tp|p=25287069|t=2014. Targeting GPR30 with G-1: a new therapeutic target for castration-resistant prostate cancer |pdf=|usr=}}{{25287069}} gab.com Text Targeting GPR30 with G-1: a new therapeutic target for castration-resistant prostate cancer JO: Endocr Relat Cancer http://www.kidney.de/pget.php?&tw=1&pmid=25287069 #FOAvip Castration-resistant prostate cancer (CRPC) is an advanced-stage prostate cancer (PC) associated with high mortality. We reported that G-1, a selective agonist of G protein-coupled receptor 30 (GPR30), inhibited PC cell growth by inducing G2 cell cycle arrest and arrested PC-3 xenograft growth. However, therapeutic actions of G-1 and their relationships with androgen in vivo are unclear. Using the LNCaP xenograft to model PC growth during androgen-sensitive (AS) versus castration-resistant (CR) phase, we found that G-1 inhibited growth of CR but not AS tumors with no observable toxicity to the host. Substantial necrosis (~65%) accompanied by marked intratumoral infiltration of neutrophils was observed only in CR tumors. Global transcriptome profiling of human genes identified 99 differential expressed genes with ?interplay between innate and adaptive immune response? as the top pathway. Quantitative-PCR confirmed upregulation of neutrophil-related chemokines and inflammation-mediated cytokines only in the G-1-treated CR tumors. Expression of murine neutrophil-related cytokines also was elevated in these tumors. GPR30 expression was significantly higher in CR than AS tumors. In cell-based experiments, androgen repressed GPR30 expression, a response reversible by anti-androgen or siRNA-induced androgen receptor silencing. Finally, in clinical specimens, 80% of CRPC metastases (n=123) express a high level of GPR30 whereas only 54% of the primary PCs (n=232) showed high GPR30 expression. Together, these results provide the first evidence that GPR30 is an androgen-repressed target and G-1 mediates the anti-tumor effect via neutrophil infiltration-associated necrosis in CRPC. Additional studies are warranted to firmly establish GPR30 as a therapeutic target in CRPC. Twit Text FOAVip Targeting GPR30 with G-1: a new therapeutic target for castration-resistant prostate cancer ????Endocr Relat Cancer http://www.kidney.de/pget.php?&tw=1&pmid=25287069 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25287069 #FOAvip English Wikipedia <ref>{{Cite pmid|25287069}}</ref> Targeting GPR30 with G-1: a new therapeutic target for castration-resistant prostate cancer #MMPMID25287069 Lam HM; Ouyang B; Chen J; Ying J; Wang J; Wu CL; Li J; Medvedovic M; Vessella RL; Ho SM Endocr Relat Cancer 2014[Dec]; 21 (6): 903-14 PMID25287069show ga Castration-resistant prostate cancer (CRPC) is an advanced-stage prostate cancer (PC) associated with high mortality. We reported that G-1, a selective agonist of G protein-coupled receptor 30 (GPR30), inhibited PC cell growth by inducing G2 cell cycle arrest and arrested PC-3 xenograft growth. However, therapeutic actions of G-1 and their relationships with androgen in vivo are unclear. Using the LNCaP xenograft to model PC growth during androgen-sensitive (AS) versus castration-resistant (CR) phase, we found that G-1 inhibited growth of CR but not AS tumors with no observable toxicity to the host. Substantial necrosis (~65%) accompanied by marked intratumoral infiltration of neutrophils was observed only in CR tumors. Global transcriptome profiling of human genes identified 99 differential expressed genes with ?interplay between innate and adaptive immune response? as the top pathway. Quantitative-PCR confirmed upregulation of neutrophil-related chemokines and inflammation-mediated cytokines only in the G-1-treated CR tumors. Expression of murine neutrophil-related cytokines also was elevated in these tumors. GPR30 expression was significantly higher in CR than AS tumors. In cell-based experiments, androgen repressed GPR30 expression, a response reversible by anti-androgen or siRNA-induced androgen receptor silencing. Finally, in clinical specimens, 80% of CRPC metastases (n=123) express a high level of GPR30 whereas only 54% of the primary PCs (n=232) showed high GPR30 expression. Together, these results provide the first evidence that GPR30 is an androgen-repressed target and G-1 mediates the anti-tumor effect via neutrophil infiltration-associated necrosis in CRPC. Additional studies are warranted to firmly establish GPR30 as a therapeutic target in CRPC. äTargeting GPR30 with G-1: a new therapeutic target for castration-resi(epmc).pdf DeepDyve Pubget Overpricing