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10.1016/j.bbrep.2016.11.004 http://scihub22266oqcxt.onion/10.1016/j.bbrep.2016.11.004 C5614541!5614541!28955990     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28955990&cmd=llinks): Failed to open stream: HTTP request failed! 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Synergistic effects of 15-deoxy ?12,14-prostaglandin J2 on the anti-tumor activity of doxorubicin in renal cell carcinoma |pdf=|usr=}}{{28955990}} gab.com Text Synergistic effects of 15-deoxy 12,14-prostaglandin J2 on the anti-tumor activity of doxorubicin in renal cell carcinoma JO: Biochem Biophys Rep http://www.kidney.de/pget.php?&tw=1&pmid=28955990 #FOAvip An endogenous anticancer agent, 15-deoxy -?12,14-prostaglandin J2 (15d-PGJ2) induces apoptosis in the chemoresistant renal cell carcinoma (RCC). Peroxisome proliferator-activated receptor-? (PPAR?) is a nuclear receptor for 15d-PGJ2, and mediates the cytotoxicity of 15d-PGJ2 in many cancerous cells. However, 15d-PGJ2 induces apoptosis independently of PPAR? in human RCC cell line such as Caki-2. In the present study, we found that 15d-PGJ2 ameliorated the chemoresistance to one of anthracycline antibiotics, doxorubicin, in Caki-2 cells. Doxorubicin alone exhibited weak cytotoxicity at the concentrations effective for other cancer cells such as Hela cells. In addition, it did not activate caspase 3. However, the cytotoxicity of doxorubicin was increased remarkably and accompanied with the caspase- 3 activation in the presence of 15d-PGJ2. Doxorubicin alone damaged plasma membrane, and the combined application of 15d-PGJ2 with doxorubicin increased the membrane permeability slightly. PPAR? was involved in neither the anti-tumor activity nor the synergistic effect of 15d-PGJ2. 15d-PGJ2 induces apoptosis in Caki-2 cells via suppressing the phosphoinositide 3-kinase (PI3K)-Akt pathway. The effect of PI3K inhibitor on the cytotoxicity of doxorubicin was additive, but not synergistic. Although the PI3K inhibitor mimicked the cytotoxicity of 15d-PGJ2, it might not be involved in the synergism between 15d-PGJ2 and doxorubicin. In conclusion, 15d-PGJ2 enhanced the chemosensitivity of doxorubicin via the pathway independent of PPAR? and PI3K. Twit Text FOAVip Synergistic effects of 15-deoxy 12,14-prostaglandin J2 on the anti-tumor activity of doxorubicin in renal cell carcinoma ????Biochem Biophys Rep http://www.kidney.de/pget.php?&tw=1&pmid=28955990 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28955990 #FOAvip English Wikipedia <ref>{{Cite pmid|28955990}}</ref> Synergistic effects of 15-deoxy ?12,14-prostaglandin J2 on the anti-tumor activity of doxorubicin in renal cell carcinoma #MMPMID28955990 Yamamoto Y; Yamamoto T; Koma H; Nishii A; Yagami T Biochem Biophys Rep 2017[Mar]; 9 (ä): 61-6 PMID28955990show ga An endogenous anticancer agent, 15-deoxy -?12,14-prostaglandin J2 (15d-PGJ2) induces apoptosis in the chemoresistant renal cell carcinoma (RCC). Peroxisome proliferator-activated receptor-? (PPAR?) is a nuclear receptor for 15d-PGJ2, and mediates the cytotoxicity of 15d-PGJ2 in many cancerous cells. However, 15d-PGJ2 induces apoptosis independently of PPAR? in human RCC cell line such as Caki-2. In the present study, we found that 15d-PGJ2 ameliorated the chemoresistance to one of anthracycline antibiotics, doxorubicin, in Caki-2 cells. Doxorubicin alone exhibited weak cytotoxicity at the concentrations effective for other cancer cells such as Hela cells. In addition, it did not activate caspase 3. However, the cytotoxicity of doxorubicin was increased remarkably and accompanied with the caspase- 3 activation in the presence of 15d-PGJ2. Doxorubicin alone damaged plasma membrane, and the combined application of 15d-PGJ2 with doxorubicin increased the membrane permeability slightly. PPAR? was involved in neither the anti-tumor activity nor the synergistic effect of 15d-PGJ2. 15d-PGJ2 induces apoptosis in Caki-2 cells via suppressing the phosphoinositide 3-kinase (PI3K)-Akt pathway. The effect of PI3K inhibitor on the cytotoxicity of doxorubicin was additive, but not synergistic. Although the PI3K inhibitor mimicked the cytotoxicity of 15d-PGJ2, it might not be involved in the synergism between 15d-PGJ2 and doxorubicin. In conclusion, 15d-PGJ2 enhanced the chemosensitivity of doxorubicin via the pathway independent of PPAR? and PI3K. äSynergistic effects of 15-deoxy ?12,14-prostaglandin J2 on the anti-tu(epmc).pdf DeepDyve Pubget Overpricing