Cargando…
TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究
BACKGROUND AND OBJECTIVE: It 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-β1) has been identified as the main inducer of tumor EMT. The aim of t...
Formato: | Online Artículo Texto |
---|---|
Lenguaje: | English |
Publicado: |
中国肺癌杂志编辑部
2010
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000676/ https://www.ncbi.nlm.nih.gov/pubmed/20672701 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.01.06 |
_version_ | 1783331810250326016 |
---|---|
collection | PubMed |
description | BACKGROUND AND OBJECTIVE: It 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-β1) has been identified as the main inducer of tumor EMT. The aim of this study was to investigate the effects of TGF-β1 on EMT and PI3K/AKT signaling pathway in lung adencarcinoma PC9 cells. METHODS: Cultured PC9 cells were treated with different concentrations of TGF-β1 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. RESULTS: The data showed that TGF-β1 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-β1 treatment for 48 h. CONCLUSION: TGF-β1 might induce EMT of PC9 cells, accompanied by the changes of PI3K/AKT signaling pathway. |
format | Online Article Text |
id | pubmed-6000676 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | 中国肺癌杂志编辑部 |
record_format | MEDLINE/PubMed |
spelling | pubmed-60006762018-07-06 TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: It 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-β1) has been identified as the main inducer of tumor EMT. The aim of this study was to investigate the effects of TGF-β1 on EMT and PI3K/AKT signaling pathway in lung adencarcinoma PC9 cells. METHODS: Cultured PC9 cells were treated with different concentrations of TGF-β1 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. RESULTS: The data showed that TGF-β1 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-β1 treatment for 48 h. CONCLUSION: TGF-β1 might induce EMT of PC9 cells, accompanied by the changes of PI3K/AKT signaling pathway. 中国肺癌杂志编辑部 2010-01-20 /pmc/articles/PMC6000676/ /pubmed/20672701 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.01.06 Text en 版权所有©《中国肺癌杂志》编辑部2010 https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/ |
spellingShingle | 基础研究 TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究 |
title | TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究 |
title_full | TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究 |
title_fullStr | TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究 |
title_full_unstemmed | TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究 |
title_short | TGF-beta1诱导人肺腺癌PC9细胞上皮-间质转化的研究 |
title_sort | tgf-beta1诱导人肺腺癌pc9细胞上皮-间质转化的研究 |
topic | 基础研究 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000676/ https://www.ncbi.nlm.nih.gov/pubmed/20672701 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.01.06 |
work_keys_str_mv | AT tgfbeta1yòudǎorénfèixiànáipc9xìbāoshàngpíjiānzhìzhuǎnhuàdeyánjiū AT tgfbeta1yòudǎorénfèixiànáipc9xìbāoshàngpíjiānzhìzhuǎnhuàdeyánjiū AT tgfbeta1yòudǎorénfèixiànáipc9xìbāoshàngpíjiānzhìzhuǎnhuàdeyánjiū AT tgfbeta1yòudǎorénfèixiànáipc9xìbāoshàngpíjiānzhìzhuǎnhuàdeyánjiū |