Research of TGF-beta1 inducing lung adencarcinoma PC9 cells to mesenchymal cells transition.
- Author:
Huijun ZHANG
1
;
Lei ZHANG
;
Heyong WANG
;
Xiaofeng CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adenocarcinoma; metabolism; pathology; Blotting, Western; Cell Differentiation; drug effects; Cell Line, Tumor; Epithelial Cells; pathology; Fibronectins; metabolism; Humans; Lung Neoplasms; metabolism; pathology; Mesoderm; metabolism; pathology; Microscopy, Phase-Contrast; Proto-Oncogene Proteins c-akt; metabolism; Signal Transduction; drug effects; Transforming Growth Factor beta1; pharmacology
- From: Chinese Journal of Lung Cancer 2010;13(1):34-37
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND AND OBJECTIVEIt has been proven that epithelial-mesenchymal transition (EMT) not only correlated with embryonic development but also could promote tumor invasion and metastasis. Transforming growth factor beta-1 (TGF-beta1) has been identified as the main inducer of tumor EMT. The aim of this study was to investigate the effects of TGF-beta1 on EMT and PI3K/AKT signaling pathway in lung adencarcinoma PC9 cells.
METHODSCultured PC9 cells were treated with different concentrations of TGF-beta1 for 48 h. The morphological changes were observed under phase-contrast microscopy; EMT relative marker protein changes were assessed by Western blot and immunoflurescence staining. In addition, the expression of AKT and P-AKT were also measured by Western blot.
RESULTSThe data showed that TGF-beta1 could induce PC9 morphological alteration from epithelial to mesenchymal and upregulate the expression of mesenchymal maker protein Fibronectin. Obviously, the expression of P-AKT was downregulated by TGF-beta1 treatment for 48 h.
CONCLUSIONTGF-beta1 might induce EMT of PC9 cells, accompanied by the changes of PI3K/AKT signaling pathway.
