奎寧抑制RAGE-STAT3調控之自體吞噬路徑以促進紫檀芪誘發之胰臟癌細胞死亡

呂懿臻

doi:10.6844/NCKU.2013.00002

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奎寧抑制RAGE-STAT3調控之自體吞噬路徑以促進紫檀芪誘發之胰臟癌細胞死亡

Chloroquine Promotes Pancreatic Cancer Cell Apoptosis Induced by Pterostilbene Through Downregulation of RAGE-STAT3 Mediated Autophagy Pathway

呂懿臻 , Masters　　Advisor：王應然　　

繁體中文 DOI： 10.6844/NCKU.2013.00002

紫檀芪；奎寧；胰臟癌；自體吞噬； Pterostilbene ； Chloroquine ； pancreatic cancer ； autophagy

Abstract │ Reference (60) │ Altmetrics

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Pancreatic cancer is reported to be the fourth leading cause of cancer death in the United States with a 5-year survival less than 5%. The common treatment is the Gemcitabine (GEM) therapy for pancreatic cancer, but pancreatic tumors are highly resistant to GEM. Previous studies have demonstrated that exposure of pancreatic tumor cells to GEM provoked a nuclear factor kappa B (NF-κB) -dependent increase in RAGE expression, and overexpression of RAGE led to greater induction of autophagy that improved tumor cell survival and chemotherapeutic resistant. Pterostilbene is a stilbenoid chemically related to resveratrol. Experimental evidence shows that Pterostilbene has potential for the prevention or treatment of cancers by inducing apoptosis or autophagy in cancer cells. Chloroquine is an effective and safe anti-malarial agent, and has the ability to inhibit autophagy. The aim of this study is to investigate whether pterostilbene combined with autophagy inhibitor Chloroquine could potentiate cell death in pancreatic cancer cells and to study the molecular anti-cancer mechanisms of pterostilbene combined with chloroquine. Cell viability was determined by MTT assay. Cell cycle, apoptosis, and autophagy were analyzed by flow cytometry. The expression of proteins that regulate apoptosis and autophagy were performed by western blotting. In in vivo study, we use orthotopic model with IVIS image system to evaluate the anti-cancer effects of pterostilbene combined with chloroquine, and further to demonstrate the related mechanisms by western blotting and immunohistochemistry. In the in vitro studies, the cell viability in MiaPaCa-2 cells were higher than BxPC-3 cells after treatment with pterostilbene. The results indicated that MiaPaCa-2 had higher autophagy. Autophagy inhibitions by chloroquine in MiaPaCa-2 significantly decreased the cell viability, and increased apoptosis that induced by pterostilbene through down regulation  of RAGE、STAT3 and AKT pathways. In the in vivo experiment, pterostilbene combined with Chloroquine has demonstrated to inhibit orthotopic pancreatic cancer growth by reducing tumor weight and tumor volume. The results indicated pterostilbene can inhibit pancreatic cancer cells growth by inducing apoptosis. Autophagy suppression by chloroquine potentiates pterostilbene induced cell death in pancreatic cancer cells through inhibiting RAGE-STAT3 pathway and AKT pathways.

Reference ( 60 ) 〈TOP〉

Alosi, J. A., D. E. McDonald, et al. (2010). "Pterostilbene inhibits breast cancer in vitro through mitochondrial depolarization and induction of caspase-dependent apoptosis." J Surg Res 161(2): 195-201.
連結：
Arumugam, T., D. M. Simeone, et al. (2005). "S100P promotes pancreatic cancer growth, survival, and invasion." Clin Cancer Res 11(15): 5356-5364.
連結：
Augustijns, P., P. Geusens, et al. (1992). "Chloroquine levels in blood during chronic treatment of patients with rheumatoid arthritis." Eur J Clin Pharmacol 42(4): 429-433.
連結：
Breckenridge, A. M. and P. A. Winstanley (1997). "Clinical pharmacology and malaria." Ann Trop Med Parasitol 91(7): 727-733.
連結：
Chen, R. J., C. T. Ho, et al. (2010). "Pterostilbene induces autophagy and apoptosis in sensitive and chemoresistant human bladder cancer cells." Mol Nutr Food Res 54(12): 1819-1832.
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