Effects of arsenic trioxide on cell cycle and expression of cyclin dependent kinase inhibitors of multiple myeloma cells.
- Author:
Yu-bao CHEN
1
;
Wei-jun FU
;
Jian HOU
;
Si-qi DING
;
Dong-xing WANG
;
Zhen-gang YUAN
;
Xian-tao KONG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; Arsenicals; pharmacology; Cell Cycle; drug effects; physiology; Cyclin-Dependent Kinase Inhibitor p15; biosynthesis; genetics; Cyclin-Dependent Kinase Inhibitor p16; biosynthesis; genetics; Cyclin-Dependent Kinase Inhibitor p21; biosynthesis; genetics; Humans; Multiple Myeloma; drug therapy; metabolism; pathology; Oxides; pharmacology; RNA, Messenger; genetics; Tumor Cells, Cultured
- From: Chinese Journal of Hematology 2003;24(4):193-196
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects of arsenic trioxide (As(2)O(3)) on cell cycle and expression of cyclin dependent kinase inhibitors (CDKIs) in multiple myeloma (MM) cells, and explore its pharmacological mechanism.
METHODSThe DNA content of MM cells line HS-Sultan was analyzed by flow cytometry after exposure to As(2)O(3), the effects on expression of CDKI P15, P16 AND P21 were studied by reverse transcriptase PCR.
RESULTSDNA flow cytometric analysis showed that As(2)O(3) induced most of HS-Sultan cells, arrest at G(0)/G(1) phase and a small fraction at G(2)/M phase and apoptosis occurred mainly in S phase. There was no expression of P15 and P16 mRNA in untreated HS-Sultan cells and 1.0 micromol/L As(2)O(3) could make them expressed after exposed 24 or 48 hours respectively. Expression of P12 mRNA was obviously elevated by As(2)O(3) comparing with that of control.
CONCLUSIONOne of the pharmacological mechanisms of As(2)O(3) is to activate the expression of CDKI P15, P16 and P21, and consequently affect cell proliferation cycle.