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Cordycepin increases sensitivity of Hep3B human hepatocellular carcinoma cells to TRAIL-mediated apoptosis by inactivating the JNK signaling pathway

Cordycepin increases sensitivity of Hep3B human hepatocellular carcinoma cells to TRAIL-mediated apoptosis by inactivating the JNK signaling pathway
Lee, HH[Lee, Hye Hyeon]Jeong, JW[Jeong, Jin-Woo]Lee, JH[Lee, Jun Hyuk]Kim, GY[Kim, Gi-Young]Cheong, J[Cheong, Jaehun]Jeong, YK[Jeong, Yong Kee]Yoo, YH[Yoo, Young Hyun]Choi, YH[Choi, Yung Hyun]
DGIST Authors
Jeong, JW[Jeong, Jin-Woo]
Issued Date
Article Type
Anthra[1,9 CD]Pyrazol 6(2H) OneAntineoplastic ActivityAntineoplastic AgentsApoptosisBeta CateninBlotting, WesternC-Jun N-Terminal KinaseCancer Cell CultureCarcinoma, HepatocellularCaspaseCaspasesCell Cycle G1 PhaseCell InfiltrationCell ProliferationChromatin CondensationConcentration ResponseControlled StudyCordycepinDeoxyadenosinesDrug SensitivityDrug TargetingEnzyme InactivationFlow CytometryHep3B CellsHumanHuman CellHumansJNK Mitogen-Activated Protein KinasesLiver Cell CarcinomaLiver NeoplasmsMembrane Potential, MitochondrialNicotinamide Adenine Dinucleotide Adenosine Diphosphate RibosyltransferasePriority JournalProtein BCL 2Protein CleavageProtein ExpressionProtein FunctionProtein Protein InteractionReal-Time Polymerase Chain ReactionReverse Transcriptase-Polymerase Chain ReactionRNA, MessengerSignal TransductionStress Activated Protein KinaseTNF-Related Apoptosis-Inducing LigandTRAILTumor Cells, CulturedTumor Necrosis Factor Related Apoptosis Inducing Ligand
Resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis has been reported in various cancer cells. Cordycepin, a specific polyadenylation inhibitor, is the main functional component in Cordyceps militaris, which possesses many pharmacological activities including antitumor and anti-inflammation. In the present study, we demonstrated that treatment of cordycepin sensitized TRAIL-resistant Hep3B human hepatocellular carcinoma cells to TRAIL-mediated apoptosis as evidenced by formation of apoptotic bodies, chromatin condensation and accumulation of cells in the sub-G1 phase. The induction of apoptosis following co-treatment with cordycepin and TRAIL in Hep3B cells appeared to be correlated with modulation of Bcl-2 family protein expression and activation of the caspase cascade, which resulted in the cleavage of poly(ADP-ribose) polymerase and β-catenin. In addition, cordycepin treatment also inhibited activation of c-Jun N-terminal kinase (JNK). Pretreatment with SP600125, a JNK inhibitor, resulted in a significantly increased sub-G1 population and caspase activity in cordycepin plus TRAIL-mediated apoptosis. Taken together, these results indicate that JNK acts as a key regulator of apoptosis in response to combined treatment with cordycepin and TRAIL in human hepatocellular carcinoma Hep3B cells.
Spandidos Publications
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