Regulatory effect of NOX-4 on PI3K signaling pathway in TGF-β1-in-duced collagen Ⅰ synthesis from lung cancer cells
10.3969/j.issn.1000-4718.2018.06.009
- VernacularTitle:NOX-4调控PI3K信号通路参与TGF-β1诱导肺癌细胞表达Ⅰ型胶原蛋白
- Author:
Nian DONG
1
;
Ya-Ni YU
;
Deng-Min WU
;
Bei-Bei WANG
;
Zhao-Jian YING
;
Dan-Ping QIU
;
Li DONG
;
Cheng-Shui CHEN
Author Information
1. 温州医科大学附属第一医院呼吸与危重症医学科
- Keywords:
Transforming growth factor-β1;
NADPH oxidase-4;
PI3K/Akt signaling pathway;
Collagen type Ⅰ;
Lung cancer
- From:
Chinese Journal of Pathophysiology
2018;34(6):1014-1019
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the regulatory effect of NADPH oxidase-4 (NOX-4) on PI3K signaling path-way in transforming growth factor-β1 (TGF-β1)-induced collagen type Ⅰ (collagen Ⅰ) synthesis from lung cancer cells and the mechanisms. METHODS:Human lung cancer A549 cells were cultured in vitro and stimulated with TGF-β1. The ex-pression of NOX family and collagen family at mRNA and protein levels as well as the PI3K class Ⅰ catalytic subunits and the activation of PI3K signaling pathway was measured. A549 cells were pre-treated with NOX-4 inhibitor diphenyleneiodo-nium (DPI), and the expression of collagen Ⅰ at mRNA level as well as the PI3K class Ⅰ catalytic subunits and the activa-tion of PI3K signaling pathway was measured upon TGF-β1 stimulation. RESULTS:TGF-β1 stimulated the expression of NOX-4 and collagen Ⅰ at mRNA and protein levels as well as the expression of PIK3CD and the activation of PI3K signaling pathway at a dose- and time-dependent manner. NOX-4 inhibitor DPI partly reversed TGF-β1-induced collagen Ⅰ expres-sion. Inhibition of NOX-4 down-regulated the degree of TGF-β1-stimulated activation of PI3K signaling pathway without effect on the expression of PIK3CD. CONCLUSION:NOX-4 participates in TGF-β1-induced collagen Ⅰ synthesis from lung cancer cells via regulating the activation of PI3K signaling pathway. TGF-β1/NOX-4/PI3K signaling pathway axis acts as a regulatory role in collagen Ⅰ synthesis from lung cancer cells.
