作者: Yuqi Shi , Zhilong He , Zhenyu Jia , Chunfang Xu
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摘要: Pancreatic cancer is a malignant digestive system tumor with particularly poor prognosis, and the fourth leading cause of cancer‑associated mortality in USA. The anti‑diabetic therapeutic agent, metformin (MET) has been demonstrated to exert anti‑tumor effects. present study assessed ability MET, alone or combination gemcitabine (GEM), inhibit growth human CFPAC‑1 pancreatic cell line in vitro in vivo. Cell counting kit‑8 assays were performed measure viability apoptosis was detected annexin V/propidium iodide. cycle analysis conducted by flow cytometry. mRNA protein levels B‑cell lymphoma‑extra large (Bcl‑xL), Bcl2 associated X (Bax), caspase‑3, survivin cyclin D1 cells tissues reverse transcription‑polymerase chain reaction western blotting, respectively. Furthermore, expression caspase‑3 proliferating nuclear antigen immunohistochemistry. results that following MET treatment, xenografts nude mice inhibited, Bcl‑xL, downregulated, while Bax upregulated. These effects enhanced when administered GEM. mechanism underlying effect may be induction inhibition proliferation.