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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]
Issued Date
Article Type
Amino Acid Chloromethyl KetonesAntineoplastic ActivityAntineoplastic AgentAntineoplastic AgentsApoptosisAutophagyBax Protein, HumanBcl-2-Associated X ProteinBenzyloxycarbonylvalyl-Alanyl-Aspartyl Fluoromethyl KetoneBH3 Interacting Domain Death Agonist ProteinBid Protein, HumanCarcinomaCaspaseCaspase 3Caspase 8Caspase 9Caspase InhibitorCaspase InhibitorsCaspasesCell DeathCell Line, TumorCell SurvivalConcentration ResponseControlled StudyCordycepinDeath Receptor 5Deoxyadenosine DerivativeDeoxyadenosinesDrug EffectsFas AntigenHumanHuman CellHumansLNCaP Cell lineLNCaP CellsMaleMetabolismMicrotubule Associated ProteinMitochondrial Membrane PotentialPeptide Chloromethyl KetonePriority JournalProstate CarcinomaProstate TumorProstatic NeoplasmsProtein BaxProtein BCL 2Protein BidProto-Oncogene Proteins C-BCL-2Tumor 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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