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PKCδ and JNK Mediates Camptothecin-induced Apoptosis in Leukemia Cell Line U937
Li Hui1*, Han Bing2
1Shanghai University of Medicine & Health Sciences, Shanghai 201318, China;
2Minhang Hospital, Fudan University, Shanghai 201199, China
2Minhang Hospital, Fudan University, Shanghai 201199, China
Abstract: The flow cytometry and Western blot were used to investigate the effect of PKCδ and JNK during camptothecin-induced apoptosis in leukemia cell line U937. The results demonstrated that under 50 nmol/L camptothecin treatment for 24 h， 36 h or 48 h， U937 cells underwent apoptosis， and PKCδ and JNK proteins were obviously activated. In addition， the pretreatment of PKCδ-specific inhibitor rottlerin significantly inhibited phosphorylation of JNK during camptothecin-induced cell death. Mostly， SP600125， a phosphorylation of JNK inhibitor， greatly blocked proteolytic cleavage of PKCδ and camptothecin-induced cell death. Accordingly， SP600125 significantly suppressed cell death in U937 cells which stably transfected with pTRE2hyg-PKCδ-CF grown in tetracycline-free medium. PKCδ and JNK may mediate camptothecin-induced cell death. These results may provide new mechanisms for camptothecininduced cancer cell death and novel therapeutic clues for cancer treatment.
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