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Involvement of autophagy in cordycepin-induced apoptosis in human prostate carcinoma LNCaP cells
- Involvement of autophagy in cordycepin-induced apoptosis in human prostate carcinoma LNCaP cells
- Lee, HH[Lee, Hye Hyeon]; Kim, SO[Kim, Sung Ok]; Kim, GY[Kim, Gi-Young]; Moon, SK[Moon, Sung-Kwon]; Kim, WJ[Kim, Wun-Jae]; Jeong, YK[Jeong, Yong Kee]; Yoo, YH[Yoo, Young Hyun]; Choi, YH[Choi, Yung Hyun]
- DGIST Authors
- Lee, HH[Lee, Hye Hyeon]
- Issue Date
- Environmental Toxicology and Pharmacology, 38(1), 239-250
- Article Type
- Amino Acid Chloromethyl Ketones; Antineoplastic Activity; Antineoplastic Agent; Antineoplastic Agents; Apoptosis; Autophagy; Bax Protein, Human; Bcl-2-Associated X Protein; Benzyloxycarbonylvalyl-Alanyl-Aspartyl Fluoromethyl Ketone; BH3 Interacting Domain Death Agonist Protein; Bid Protein, Human; Carcinoma; Caspase; Caspase 3; Caspase 8; Caspase 9; Caspase Inhibitor; Caspase Inhibitors; Caspases; Cell Death; Cell Line, Tumor; Cell Survival; Concentration Response; Controlled Study; Cordycepin; Death Receptor 5; Deoxyadenosine Derivative; Deoxyadenosines; Drug Effects; Fas Antigen; Human; Human Cell; Humans; LNCaP Cell line; LNCaP Cells; Male; Metabolism; Microtubule Associated Protein; Mitochondrial Membrane Potential; Peptide Chloromethyl Ketone; Priority Journal; Prostate Carcinoma; Prostate Tumor; Prostatic Neoplasms; Protein Bax; Protein BCL 2; Protein Bid; Proto-Oncogene Proteins C-BCL-2; Tumor Cell Line
- Cordycepin treatment caused a dose-dependent increase of pro-apoptotic Bax and decrease of anti-apoptotic Bcl-2, triggering collapse of the mitochondrial membrane potential and activation of caspase-9 and -3. Cordycepin-induced cell death was also associated with induction of Fas and death receptor 5, activation of caspase-8, and truncation of Bid (tBid), suggesting that tBid might serve to connect activation of both the mitochondrial-mediated intrinsic and death receptor-mediated extrinsic apoptotic pathways. The general caspase inhibitor, z-VAD-fmk, completely abolished cordycepin-induced cell death, demonstrating that cordycepin-induced apoptosis was dependent on the activation of caspases. Cordycepin also stimulated autophagy, which was evidenced by an increase in microtubule-associated protein light chain-3 (LC3) puncta, accumulation of LC3-II, and elevation of autophagic flux; however, blockage of autophagic flux by the autophagic inhibitor bafilomycin A1 promoted cell-switching to apoptotic cell death. These findings suggest that cordycepin-induced autophagy functions as a survival mechanism and that autophagy is a potential strategy for treating prostate cancer that is resistant to pro-apoptotic therapeutics. © 2014 Elsevier B.V.
- Elsevier B.V.
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- ETC1. Journal Articles
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