title: The cytotoxicity of Scytosiphon lomentaria against HL-60 promyelocytic leukemia cells.
abstract: This study examined the cytotoxicity of Scytosiphon lomentaria, using various cancer cell lines. The ethyl acetate (EtOAc) fraction of this alga showed the cytotoxicity to leukemia cells, including HL-60. When HL-60 cells were treated with its EtOAc fraction, several apoptotic characteristics, such as DNA fragmentation, chromatin condensation, and an increase of the population of sub-G1 hypodiploid cells, were observed. Moreover, the EtOAc fraction decreased c-Myc expression in a dose-dependent manner. In order to understand the mechanism of apoptosis induction by S. lomentaria, we examined the changes of Bcl-2 and Bax protein expression levels. The EtOAc fraction reduced Bcl-2, an antiapoptotic protein, but increased Bax, a proapoptotic protein, in a dose-dependent manner. When we examined the activation of caspase-3, an effector of apoptosis, the expression of the active form (19 kDa) of caspase-3 increased, and the increase of their activities was demonstrated by the cleavage of poly (ADP-ribose) polymerase, a substrate of caspase-3, to 85 kDa. The results suggest that the inhibitory effect of S. lomentaria on the growth of HL-60 appears to arise from the induction of apoptosis by way of the down-regulation of Bcl-2 and the activation of caspase.
authors.affiliation: Department of Medicine, College of Medicine, Cheju National University, Ara 1-dong, Jeju 690-756, South Korea.
authors.forename: Sang-Cheol
authors.initials: SC
authors.lastname: Kim
authors.forename: Soo-Young
authors.initials: SY
authors.lastname: Park
authors.forename: Jae-Hee
authors.initials: JH
authors.lastname: Hyoun
authors.forename: Heeyeong
authors.initials: H
authors.lastname: Cho
authors.forename: Ji-Hoon
authors.initials: JH
authors.lastname: Kang
authors.forename: Young-Ki
authors.initials: YK
authors.lastname: Lee
authors.forename: Doek-Bae
authors.initials: DB
authors.lastname: Park
authors.forename: Eun-Sook
authors.initials: ES
authors.lastname: Yoo
authors.forename: Hee-Kyoung
authors.initials: HK
authors.lastname: Kang
mesh_terms: D000085:Acetates / Q000494:pharmacology*; D017209:Apoptosis; D015153:Blotting, Western; D053148:Caspase 3; D020169:Caspases / Q000096:biosynthesis; D002467:Cell Nucleus / Q000378:metabolism; D002843:Chromatin / Q000187:drug effects; D004247:DNA / Q000187:drug effects; D053938:DNA Fragmentation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D004789:Enzyme Activation; D004791:Enzyme Inhibitors; D056890:Eukaryota / Q000378:metabolism*; D016193:G1 Phase; D015972:Gene Expression Regulation, Neoplastic; D018922:HL-60 Cells; D006801:Humans; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D016271:Proto-Oncogene Proteins c-myc / Q000096:biosynthesis; D013997:Time Factors; D051028:bcl-2-Associated X Protein
chemical_list: D000085:Acetates; C494826:BAX protein, human; D002843:Chromatin; D004791:Enzyme Inhibitors; D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc; D051028:bcl-2-Associated X Protein; C007650:ethyl acetate; D004247:DNA; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases