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P53 is required for Doxorubicin-induced apoptosis via the TGF-beta signaling pathway in osteosarcoma-derived cells |pdf=|usr=}}{{27073729 }} gab.com Text P53 is required for Doxorubicin-induced apoptosis via the TGF-beta signaling pathway in osteosarcoma-derived cells JO: Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27073729 #FOAvip Osteosarcoma is the most common type of aggressive bone cancer. Current treatment strategies include surgical resection, radiation, and chemotherapy. Doxorubicin has been widely used as a chemotherapeutic drug to treat osteosarcoma. However, drug resistance has become a challenge to its use. In this study, p53-wild type U2OS and p53-null MG-63 osteosarcoma-derived cells were used to investigate the mechanism of doxorubicin-induced cytotoxicity. In cell viability assays, doxorubicin effectively induced apoptosis in U2OS cells via the p53 signaling pathway, evidenced by elevated PUMA and p21 protein levels and activated caspase 3 cleavage. In contrast, p53-null MG-63 cells were resistant to doxorubicin-induced apoptosis, while exogenous expression of p53 increased drug sensitivity in those cells. The role of TGF-?/Smad3 signaling was investigated by using TGF-? reporter luciferase assays. Doxorubicin was able to induce TGF-? signal transduction without increasing TGF-? production in the presence of p53. Knockdown of Smad3 expression by small hairpin RNA (shRNA) showed that Smad3 was required for p53-mediated TGF-? signaling in response to doxorubicin treatment in U2OS and MG-63 cells. Taken together, these data demonstrate that p53 and TGF-?/Smad3 signaling pathways are both essential for doxorubicin-induced cytotoxicity in osteosarcoma cells. Twit Text FOAVip P53 is required for Doxorubicin-induced apoptosis via the TGF-beta signaling pathway in osteosarcoma-derived cells ????Am J Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27073729 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27073729 #FOAvip English Wikipedia <ref>{{Cite pmid|27073729 }}</ref> P53 is required for Doxorubicin-induced apoptosis via the TGF-beta signaling pathway in osteosarcoma-derived cells #MMPMID27073729 Sun Y ; Xia P ; Zhang H ; Liu B ; Shi Y Am J Cancer Res 2016[]; 6 (1 ): 114-25 PMID27073729 show ga Osteosarcoma is the most common type of aggressive bone cancer. Current treatment strategies include surgical resection, radiation, and chemotherapy. Doxorubicin has been widely used as a chemotherapeutic drug to treat osteosarcoma. However, drug resistance has become a challenge to its use. In this study, p53-wild type U2OS and p53-null MG-63 osteosarcoma-derived cells were used to investigate the mechanism of doxorubicin-induced cytotoxicity. In cell viability assays, doxorubicin effectively induced apoptosis in U2OS cells via the p53 signaling pathway, evidenced by elevated PUMA and p21 protein levels and activated caspase 3 cleavage. In contrast, p53-null MG-63 cells were resistant to doxorubicin-induced apoptosis, while exogenous expression of p53 increased drug sensitivity in those cells. The role of TGF-?/Smad3 signaling was investigated by using TGF-? reporter luciferase assays. Doxorubicin was able to induce TGF-? signal transduction without increasing TGF-? production in the presence of p53. Knockdown of Smad3 expression by small hairpin RNA (shRNA) showed that Smad3 was required for p53-mediated TGF-? signaling in response to doxorubicin treatment in U2OS and MG-63 cells. Taken together, these data demonstrate that p53 and TGF-?/Smad3 signaling pathways are both essential for doxorubicin-induced cytotoxicity in osteosarcoma cells. äP53 is required for Doxorubicin-induced apoptosis via the TGF-beta sig(epmc).pdf DeepDyve Pubget Overpricing