Apoptosis inducing effects of 6-methoxydihydrosanguinarine in HT29 colon carcinoma cells

被引:21
作者
Lee, YJ
Yin, HQ
Kim, YH
Li, GY
Lee, BH
机构
[1] Wonkwang Univ, Coll Pharm, Iksan 570749, Jeonbuk, South Korea
[2] Wonkwang Univ, MeRRI, Iksan 570749, Jeonbuk, South Korea
[3] Chungnam Natl Univ, Coll Pharm, Taejon, South Korea
关键词
6-methoxydihydrosanguinarine; Hylomecon hylomeconoides; apoptosis; HT29;
D O I
10.1007/BF02975890
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
6-Methoxydihydrosanguinarine (6WE), a benzophenanthridine alkaloid derived from the methanol extracts of Hylomecon hylomeconoides, showed a dose-dependent effect at 1-10 muM on causing apoptotic cell death in HT29 colon carcinoma cells (IC50 = 5.0 +/- 0.2 muM). Treatment of HT-29 cells with 6ME resulted in the formation of internucleosomal DNA fragmentation. Treatment of the cells with 6ME caused activation of caspase-3, -8 and 9 protease and subsequent proteolytic cleavage of poly(ADP-ribose)polymerase. 6ME increased the expression of p53 and Bax and decreased the expression of Bid. These results indicate that p53 and proapoptotic Bcl-2 family proteins might participate in the antiproliferative activity of 6ME in HT29 cells.
引用
收藏
页码:1253 / 1257
页数:5
相关论文
共 14 条
[1]   A new tetrahydroprotoberberine N-oxide alkaloid and anti-platelet aggregation constituents of Corydalis tashiroi [J].
Chen, JJ ;
Chang, YL ;
Teng, CM ;
Lin, WY ;
Chen, YC ;
Chen, IS .
PLANTA MEDICA, 2001, 67 (05) :423-427
[2]  
CHO YS, 2001, THESIS CHUNGNAM NATL
[3]   The antioxidant 4b,5,9b,10-tetrahydroindeno[1,2-b]indole inhibits apoptosis by preventing caspase activation following mitochondrial depolarization [J].
Devitt, GP ;
Creagh, EM ;
Cotter, TG .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 264 (03) :622-629
[4]   TREATMENT OF COLONIC AND RECTAL ADENOMAS WITH SULINDAC IN FAMILIAL ADENOMATOUS POLYPOSIS [J].
GIARDIELLO, FM ;
HAMILTON, SR ;
KRUSH, AJ ;
PIANTADOSI, S ;
HYLIND, LM ;
CELANO, P ;
BOOKER, SV ;
ROBINSON, CR ;
OFFERHAUS, GJA .
NEW ENGLAND JOURNAL OF MEDICINE, 1993, 328 (18) :1313-1316
[5]   Cancer statistics, 2000 [J].
Greenlee, RT ;
Murray, T ;
Bolden, S ;
Wingo, PA .
CA-A CANCER JOURNAL FOR CLINICIANS, 2000, 50 (01) :7-33
[6]   Cellular stress response and apoptosis in cancer therapy [J].
Herr, I ;
Debatin, KM .
BLOOD, 2001, 98 (09) :2603-2614
[7]   Caspase-3 is required for DNA fragmentation and morphological changes associated with apoptosis [J].
Jänicke, RU ;
Sprengart, ML ;
Wati, MR ;
Porter, AG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (16) :9357-9360
[8]   Essential requirement for caspase-8/FLICE in the initiation of the Fas-induced apoptotic cascade [J].
Juo, P ;
Kuo, CJ ;
Yuan, JY ;
Blenis, J .
CURRENT BIOLOGY, 1998, 8 (18) :1001-1008
[9]   CYTOTOXICITY-DEPENDENT APO-1 (FAS/CD95)-ASSOCIATED PROTEINS FORM A DEATH-INDUCING SIGNALING COMPLEX (DISC) WITH THE RECEPTOR [J].
KISCHKEL, FC ;
HELLBARDT, S ;
BEHRMANN, I ;
GERMER, M ;
PAWLITA, M ;
KRAMMER, PH ;
PETER, ME .
EMBO JOURNAL, 1995, 14 (22) :5579-5588
[10]   Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c [J].
Korsmeyer, SJ ;
Wei, MC ;
Saito, M ;
Weller, S ;
Oh, KJ ;
Schlesinger, PH .
CELL DEATH AND DIFFERENTIATION, 2000, 7 (12) :1166-1173