- Author:
Fan-Ping WANG
1
,
2
;
Jing-Jing ZHANG
3
;
Li-Min FANG
3
;
Ya-Li ZHANG
3
;
Lu-Lu CHEN
3
;
Yue-Yuan ZHANG
3
;
Jun-Peng LI
4
;
Ming-Yong WANG
5
Author Information
- Publication Type:Journal Article
- From: Journal of Experimental Hematology 2016;24(6):1725-1729
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of arsenic trioxide (AsO) on K562 cell proliferation by regulating cell cycle protein D1 and cyclin-dependent kinase inhibitor p27kip1.
METHODSMTT was used to detect the effect of AsOon K562 cell proliferation, so as to screen out the appropriate drug concentration. Furthermore, the K562 cell apoptosis was observed by microscopy. The expression of CyclinD1 and p27kip1 in K562 cells treated with AsOwas analyzed by reverse transcription-polymerase chain reaction(RT-PCR), immunohistochemistry and Western blot.
RESULTSAsOcould inhibit the proliferation of K562 cells in a dose- and time- dependent manner (r= 0.967). And the apoptosis cell number in AsOgroup was significantly higher than that in the control group(P<0.05). AsOcould markedly inhibit the expression of CyclinD1 in K562 cells(P<0.05), but the expression of P27kip1 was not significantly changed after AsOtreatment.
CONCLUSIONSAsOcan induce K562 cell apoptosis and inhibit K562 cell proliferation by regulating the expression of CyclinD1.