Effect of triptolide on the proliferation and apoptosis and on Wnt/β-catenin pathway in imatanib resistant CML cell
10.3760/cma.j.issn.1008-1372.2016.04.023
- VernacularTitle:雷公藤甲素对K562/G01细胞增殖抑制及Wnt/β-catenin通路相关机制的作用
- Author:
Wenting WEI
;
Liangming MA
- Publication Type:Journal Article
- Keywords:
TRIPTOLIDE/PD;
Leukemia,myelogenous,chronic,BCR-ABL positive/DT/ME;
Cell proliferation/DE;
Wnt proteins/ME;
beta catenin/ME
- From:
Journal of Chinese Physician
2016;18(4):575-578
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the impact of triptolide (TP) on proliferation and apoptosis of imatanib resistant CML cell (K562/G01) and its regulating effect on Wnt/β3-catenin signal pathway.Methods A series of 10,20,40,and 80 nmol/L of triptolide were used in CML cells K562/G01 for 12,24,and 48 hours.The cell proliferation was detected with methyl thiazolyl tetrazolium (MTT) test.The apoptosis was assessed with flow cytometry (FCM).The mRNA expressions of breakpoint cluster region-c-abl (BCR-ABL),β-catenin and its down-stream targets Lef-1,and cyclinD1 were analyzed with real-time quantitative polymerase chain reaction (RT-PCR),respectively.Results Triptolide significantly inhibited K562/G01 cell growth ability and induced apoptosis in a dose-dependent manner.Mter being treated with 20,40 nmol/L TP for 24 hours,the cell growth inhibition rates were (22.62 ± 1.33) ％,and (51.41 ±1.39) ％,respectively.The late apuptosis rates were (6.91 ± 0.14) ％,and (7.64 ± 0.47) ％,respectively.Meanwhile,PCR data showed that the mRNA levels of BCR-ABL were decreased,compared to the control group,the mRNA levels of β-catenin,Lef-1,and cyclinD1 were also decreased obviously after treatment.Conclusions Our data indicated that the triptolide could inhibit the proliferation and induce the apoptosis of K562/G01,and the mechanism might be related to the blockade of Wnt/β-catenin signal pathway.
