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白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭

BACKGROUND AND OBJECTIVE: Invasion and metastasis are the primary causes of death in patients with pulmonary carcinoma. The epidermal growth factor (EGF) stimulates A549 cells invasion greatly through activating ERK and PI3K-Akt signaling pathway. The aim of this study is to elucidate the inhibitory...

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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/PMC6000422/
https://www.ncbi.nlm.nih.gov/pubmed/20677551
http://dx.doi.org/10.3779/j.issn.1009-3419.2010.04.03
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collection PubMed
description BACKGROUND AND OBJECTIVE: Invasion and metastasis are the primary causes of death in patients with pulmonary carcinoma. The epidermal growth factor (EGF) stimulates A549 cells invasion greatly through activating ERK and PI3K-Akt signaling pathway. The aim of this study is to elucidate the inhibitory effect of Resveratrol on EGF-induced invasive ability of A549 cells in vitro and explore the molecular mechanism. METHODS: The cytotoxicity of Resveratrol was evaluated by methyl thiazolyltetrazolium (MTT) assay. Then, the A549 cells were treated with EGF and non-cytotoxic concentration of Resveratrol. The cells' invasion were detected by Boyden chamber assay; MMP-2 activity was determined by gelatine zymography assay; the changes of the related proteins were detected by Western blot. RESULTS: Resveratrol was not toxic to A549 cells at the concentration between 0 to 30 μM. The invasion ability of EGF-induced A549 cells was decreased after treatment with 20 μM resveratrol for 24 h, accompanied by the inhibition of MMP-2 secretion. And the levels of p-ERK1/2, PI3K (within 6 h) were suppressed too. CONCLUSION: 20 μM Resveratrol inhibits A549 cells' invasion possibly through the suppression of the activation of ERK and PI3K-Akt signaling pathways, subsequently exerting inhibitory effect on MMP-2.
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spelling pubmed-60004222018-07-06 白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Invasion and metastasis are the primary causes of death in patients with pulmonary carcinoma. The epidermal growth factor (EGF) stimulates A549 cells invasion greatly through activating ERK and PI3K-Akt signaling pathway. The aim of this study is to elucidate the inhibitory effect of Resveratrol on EGF-induced invasive ability of A549 cells in vitro and explore the molecular mechanism. METHODS: The cytotoxicity of Resveratrol was evaluated by methyl thiazolyltetrazolium (MTT) assay. Then, the A549 cells were treated with EGF and non-cytotoxic concentration of Resveratrol. The cells' invasion were detected by Boyden chamber assay; MMP-2 activity was determined by gelatine zymography assay; the changes of the related proteins were detected by Western blot. RESULTS: Resveratrol was not toxic to A549 cells at the concentration between 0 to 30 μM. The invasion ability of EGF-induced A549 cells was decreased after treatment with 20 μM resveratrol for 24 h, accompanied by the inhibition of MMP-2 secretion. And the levels of p-ERK1/2, PI3K (within 6 h) were suppressed too. CONCLUSION: 20 μM Resveratrol inhibits A549 cells' invasion possibly through the suppression of the activation of ERK and PI3K-Akt signaling pathways, subsequently exerting inhibitory effect on MMP-2. 中国肺癌杂志编辑部 2010-04-20 /pmc/articles/PMC6000422/ /pubmed/20677551 http://dx.doi.org/10.3779/j.issn.1009-3419.2010.04.03 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
白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭
title 白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭
title_full 白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭
title_fullStr 白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭
title_full_unstemmed 白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭
title_short 白藜芦醇抑制EGF诱导人肺腺癌A549细胞侵袭
title_sort 白藜芦醇抑制egf诱导人肺腺癌a549细胞侵袭
topic 基础研究
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6000422/
https://www.ncbi.nlm.nih.gov/pubmed/20677551
http://dx.doi.org/10.3779/j.issn.1009-3419.2010.04.03
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