The cytotoxicity of Scytosiphon lomentaria against HL-60 promyelocytic leukemia cells

被引:4
作者
Kim, SC
Park, SY
Hyoun, JH
Cho, HY
Kang, JH
Lee, YK
Park, DB
Yoo, ES
Kang, HK
机构
[1] Cheju Natl Univ, Coll Med, Dept Med, Cheju 690756, South Korea
[2] Korea Res Inst Chem Technol, Pharmaceut Screening Team, Taejon 305600, South Korea
关键词
Scytosiphon lomentaria; HL-60; apoptosis; c-Myc; Bcl-2; Bax; caspase-3;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 firagmentation, 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.
引用
收藏
页码:641 / 648
页数:8
相关论文
共 31 条
  • [1] ASIEDU C, 1995, CANCER RES, V55, P101
  • [2] BAFFY G, 1993, J BIOL CHEM, V268, P6511
  • [3] Apoptosis, cancer and cancer therapy
    Bold, RJ
    Termuhlen, PM
    McConkey, DJ
    [J]. SURGICAL ONCOLOGY-OXFORD, 1997, 6 (03): : 133 - 142
  • [4] BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
  • [5] OXIDATIVE STRESS AS A MEDIATOR OF APOPTOSIS
    BUTTKE, TM
    SANDSTROM, PA
    [J]. IMMUNOLOGY TODAY, 1994, 15 (01): : 7 - 10
  • [6] CARMICHAEL J, 1987, CANCER RES, V47, P936
  • [7] EFFECTS OF ACTIVATORS OF PROTEIN-KINASE C, INCLUDING BRYOSTATIN-1 AND BRYOSTATIN-2, ON THE GROWTH OF A549 HUMAN-LUNG CARCINOMA-CELLS
    DALE, IL
    GESCHER, A
    [J]. INTERNATIONAL JOURNAL OF CANCER, 1989, 43 (01) : 158 - 163
  • [8] Distelhorst CW, 1996, ONCOGENE, V12, P2051
  • [9] FERNANDESALNEMRI T, 1994, J BIOL CHEM, V269, P30761
  • [10] Proteins of the Myc network: Essential regulators of cell growth and differentiation
    Henriksson, M
    Luscher, B
    [J]. ADVANCES IN CANCER RESEARCH, VOL 68, 1996, 68 : 109 - 182