title: Study on human promyelocytic leukemia HL-60 cells apoptosis induced by fucosterol.
abstract: In this study, we investigated the effect of fucosterol on HL-60 and the molecular mechanism. HL-60 Cells were treated with fucosterol, and 3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) method was used to study fucosterol anti-tumor activity. Morphology of HL-60 cells was observed. Flow cytometry (FCM) was employed to detect the cell cycle. Laser scanning confocal microscope (LSCM) was used to analyze mitochondrial membrane potential (MMP) and the expressions of Fas, FasL, Fadd and Caspase-8. Western blot was performed to analyze the expressions of Cyt-C, Pro-Caspase-9 and Pro-Caspase-3. Caspase activity kits were used to determine the activity of Caspase-9, Caspase-8 and Caspase-3. The results showed fucosterol could inhibit the growth of HL-60 cells, and the cell cycle was arrested at G2/M phase. HL-60 cells showed obvious apoptosis morphology. After being treated with fucosterol for 24 h, HL-60 cells decreased MMP, induced Cyt-C release and Caspase-9, Caspase-3 activation. Fucosterol also increased the protein expression of Fas, FasL, Fadd and Caspase-8. Moreover, the activity of Caspase-9, Caspase-8 and Caspase-3 was increased significantly. In conclusion, Fucosterol can induce HL-60 cells apoptosis, suggesting that it may be a potent agent for cancer prevention and treatment.
authors.affiliation: Engineering Research Center of Natural Anticancer Drugs, Ministry of Education, Harbin University of Commerce, Harbin, China.
authors.forename: Yu-Bin
authors.initials: YB
authors.lastname: Ji
authors.forename: Chen-Feng
authors.initials: CF
authors.lastname: Ji
authors.forename: Lei
authors.initials: L
authors.lastname: Yue
mesh_terms: D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D002453:Cell Cycle; D053222:Fas Ligand Protein / Q000378:metabolism; D053200:Fas-Associated Death Domain Protein / Q000378:metabolism; D015973:Gene Expression Regulation, Leukemic; D018922:HL-60 Cells; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000188:drug therapy / Q000473:pathology; D053078:Membrane Potential, Mitochondrial; D018613:Microscopy, Confocal; D008856:Microscopy, Fluorescence; D013265:Stigmasterol / Q000031:analogs & derivatives* / Q000737:chemistry; D019014:fas Receptor / Q000378:metabolism
chemical_list: C505533:FADD protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D053200:Fas-Associated Death Domain Protein; D019014:fas Receptor; C015896:fucosterol; D013265:Stigmasterol; C505407:CASP3 protein, human; C505530:CASP8 protein, human; C506433:CASP9 protein, human; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9
keywords: Fucosterol; Human promyelocytic leukemia; apoptosis; mechanism