Pancreatic cancer is the fourth most common cause of cancer-relative mortality in the Western world. Gemcitabine (GEM) is the first-line standard chemotherapy used for the treatment of pancreatic cancer; however, chemoresistance to GEM remains the major obstacle to the successful control of this disease. Phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway is important in cell proliferation and survival, and it is frequently and aberrantly activated in pancreatic adenocarcinoma. Potential antitumor effects of NVPBEZ235, a PI3K/Akt inhibitor, together with a key clinically relevant antitumor agent (GEM) have been reported in a human pancreatic cancer xenograft mouse model. However, the precise molecular mechanism causing antitumor effects by NVP-BEZ235 and GEM has not been well elucidated. In this study, the authors investigated the molecular mechanism of NVP-BEZ235 plus GEM in reducing tumor cell survival in human pancreatic cancer cell lines. the study showed that the combination ofNVP-BEZ235 and GEM demonstrated synergistic antitumor effects on pancreatic cancer cells (AsPC-l, Colo-357 va BxPC-3) by inhibition of cell survival and induction of apoptotic cell death, and NVP-BEZ235 also inhibited the phosphorylation of Akt and BAD induced by GEM. the work is under way to elucidate the molecular mechlmism(s) by which NVPBEZ235 in combine with GEM enhance their antitumor effects in pancreatic cancer treatment.
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