ABSTRACT
AIM: To investigate the mechanism of apoptosis of HL60 cells induced by the annonaceous acetogenin, squamocin. METHODS: Induction of apoptosis was determined through Hoechst33258 dye staining and DNA agarose gel electrophoresis. Expression of the proteins was detected using Western blot analysis. Caspase-3 activity was detected using caspase-3 kit. RESULTS: Treatment of HL-60 cells with squamocin resulted in extensive nuclear condensation, DNA fragmentation, cleavage of the death substrate poly(ADP-ribose) polymerase (PARP) and induction of caspase-3 activity. Pretreatment of HL-60 cells with caspase-3 specific inhibitor DEVD-CHO prevented squamocin-induced DNA fragmentation, PARP cleavage and cell death. Stress-activated protein kinase (SAPK/JNK) was activated after treatment with squamocin in HL-60 cells. CONCLUSION: These results suggest that apoptosis of HL-60 cells induced by squamocin require caspase-3 activation, and could be related to SAPK activation.
Subject(s)
Apoptosis , Caspases/metabolism , Furans/pharmacology , Lactones/pharmacology , Annona/chemistry , Antineoplastic Agents, Phytogenic/isolation & purification , Antineoplastic Agents, Phytogenic/pharmacology , Caspase 3 , Drugs, Chinese Herbal/isolation & purification , Drugs, Chinese Herbal/pharmacology , Furans/isolation & purification , HL-60 Cells , Humans , Lactones/isolation & purification , Plants, Medicinal/chemistryABSTRACT
Blood selenium concentrations in 111 nasopharyngeal cancer patients and 56 normal subjects were determined using a modified 2,3-diamino naphthalene fluorometric method. Cancer subjects in this study were divided into two groups and blood Se levels (mean +/- SD) were 0.105 +/- 0.024 for untreated cases, 0.113 +/- 0.034 for those who had received treatment, and 0.109 +/- 0.030 microgram/ml for all subjects. The results suggest that low blood Se levels in nasopharyngeal cancer patients are a consequence of their disease rather than the cause of the cancer.