Effect of TGF-β1/SMAD signaling pathway on K562 cells growth inhibition caused by HMBA
10.3760/cma.j.issn.1673-422X.2010.04.024
- VernacularTitle:转化生长因子β1/SMAD信号通路在六亚甲基二乙酰胺抑制K562细胞增殖中的作用
- Author:
Enyu SU
;
Peie WEN
;
Xia REN
;
Xiaobai SUN
;
Henglan ZHANG
;
Tianhua TANG
;
Haiquan REN
;
Guosheng JIANG
- Publication Type:Journal Article
- Keywords:
Transforming growth factor betal;
SMAD proteins;
K562 cells;
Hexamethylene bisacetamide
- From:
Journal of International Oncology
2010;37(4):312-315
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of TGF-β1/SMAD signaling pathway on K562 cells growth inhibition caused by HMBA. Methods After establishing the in vitro differentiation model with HMBA on K562 cells, the MTT assay was used to detect the proliferation of K562 cells, the cell cycle profile was detected by flow cytometry, and the mRNA expression of TGF-β1, SMAD3, SMAD4 and EVI1 was measured by RT-PCR assay. Results HMBA could inhibit the proliferation and promote the differentiation of K562 cells obviously, which was time and concentration-dependent, and the 72 h corresponding IC50, was about 2 mmol/L. Within 72 h, flow cytometry assay indicated that the ration of G0-G1 phase cells was up-regulated, and the results of RT-PCR showed that relative mRNA expression of TGF-β1, SMAD3 and SMAD4 at mRNA level was increased gradually while that of EVI1 was decreased gradually. Conclusion HMBA can inhibit K562 cells proliferation through TGF-β1/SMAD signaling pathway.