Effect of NPM1 mutant A on TGF-β1-induced K562 cell proliferation and AKT phos-phorylation
10.3969/j.issn.1000-8179.2019.04.319
- VernacularTitle:NPM1 A型突变体对TGF-β1诱导K562细胞增殖及AKT磷酸化的影响*
- Author:
Zhengcai WU
1
;
Chengyan WANG
;
Xiangxin WU
;
Changsheng XU
;
Minhui LIN
Author Information
1. 福建医科大学实验动物中心(福州市350122)
- Keywords:
nucleophosmin 1 (NPM1);
K562 cells;
TGF-β1;
P-AKT;
cell proliferation
- From:
Chinese Journal of Clinical Oncology
2019;46(4):164-168
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of nucleophosmin 1 (NPM1) mutant A on TGF-β1-induced K562 cell proliferation and AKT phosphorylation. Methods: K562 cells were infected with Ad5-NPM1 to create an NPM1 over-expression cell model. NPM1 levels were determined by ELISA and Western blot analysis. The levels of AKT and P-AKT were determined by Western blot. MTT was used to measure the proliferation of K562 cells. Results: NPM1 protein levels in K562 cells increased in an Ad5-NPM1-MOI-dependent manner. Cell proliferation and NPM1 levels in the supernatant were significantly increased in K562 cells infected with Ad5-NPM1-30 and Ad5-NPM1-100 compared to those infected with Ad5-vector-100 (P<0.01). Treatment with (10 ng/mL) TGF-β1 increased P-AKT levels, but not total AKT levels in K562 cells. TGF-β1-induced phosphorylation of AKT was significantly increased by infection of K562 cells with Ad5-NPM1-100. No significant differences were found in total AKT levels among all groups. TGF-β1 (10 ng/mL) treatment also in-creased the proliferation of K562 cells. TGF-β1-induced K562 cell proliferation was significantly increased by infection with Ad5-NPM1-100 (P<0.01). Conclusions: NPM1 improves TGF-β1-induced cell proliferation by up-regulating AKT phosphorylation levels.
