Effect of curcumin on expression of survivin, Bcl-2 and Bax in human multiple myeloma cell line.
- Author:
Bo LIU
1
;
Qing-Xian BAI
;
Xie-Qun CHEN
;
Guang-Xun GAO
;
Hong-Tao GU
Author Information
1. Department of Hematology, Xijing Hospital, The Fourth Medical University, Xi'an 210032, China.
- Publication Type:Journal Article
- MeSH:
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Curcumin;
pharmacology;
Humans;
Inhibitor of Apoptosis Proteins;
Microtubule-Associated Proteins;
metabolism;
Multiple Myeloma;
metabolism;
pathology;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
RNA, Messenger;
metabolism
- From:
Journal of Experimental Hematology
2007;15(4):762-766
- CountryChina
- Language:Chinese
-
Abstract:
To explore the mechanisms of suppression growth and induction apoptosis of curcumin on human multiple myeloma cell line RPMI8226, the suppressive effect of curcumin on RPMI8226 was examined by MTT assay; the induction apoptosis and cell cycle arrest of curcumin on RPMI8226 were determined by flow cytometry (FCM); the changes of survivin, Bcl-2, Bax mRNA levels were detected by RT-PCR. The results showed that curcumin obviously suppressed the proliferation of RPMI8226 in both time- and dose-dependent manners, and the IC(50) were 12.15 micromol/L, 4.9 micromol/L for 24 and 48 hours respectively. FCM indicated that the apoptosis ratio rose from 10.6% of untreated cells up to 36.9% of treated cells (p < 0.05), and curcumin arrested cell cycle of RPMI8226 at G(2)/M phase. RT-PCR showed that RPMI8226 cells expressed survivin, Bcl-2 strongly and Bax slightly; while RPMI8226 cells were treated with curcumin 10 micromol/L for 24 hours, the expressions of survivin, Bcl-2 mRNA were apparently down-regulated, and the expression of Bax mRNA was markedly up-regulated. It is concluded that curcumin can suppress the proliferation of human multiple myeloma cell line RPMI8226, and induce their apoptosis. The mechanism of antitumous effect of curcumin may be related to down-regulation of survivin, Bcl-2 mRNA and up-regulation of Bax mRNA.
