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Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901

BACKGROUND/OBJECTIVE: To investigate the crosstalk between epidermal growth factor receptor (EGFR) and integrin-mediated signal transduction pathways in human gastric adenocarcinoma cells. METHODS: EGF was used as a ligand of EGFR to stimulate the gastric adenocarcinoma cell, SGC7901. Signal molecul...

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Detalles Bibliográficos
Autores principales: Dan, Li, Jian, Ding, Na, Lin, Xiaozhong, Wang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481856/
https://www.ncbi.nlm.nih.gov/pubmed/23109808
http://dx.doi.org/10.2147/OTT.S35322
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author Dan, Li
Jian, Ding
Na, Lin
Xiaozhong, Wang
author_facet Dan, Li
Jian, Ding
Na, Lin
Xiaozhong, Wang
author_sort Dan, Li
collection PubMed
description BACKGROUND/OBJECTIVE: To investigate the crosstalk between epidermal growth factor receptor (EGFR) and integrin-mediated signal transduction pathways in human gastric adenocarcinoma cells. METHODS: EGF was used as a ligand of EGFR to stimulate the gastric adenocarcinoma cell, SGC7901. Signal molecules downstream of the integrin, FAK(Y397) and p130cas(Y410) phosphorylation, were measured by immunoprecipitation and western blot. Fibronectin (Fn) was used as a ligand of integrin to stimulate the same cell line. Signal molecules downstream of EGFR and extracellular signal-regulated kinase (ERK) general phosphorylation were also measured. Focal adhesion kinase (FAK) small-interfering RNA was designed and transfected into SGC7901 cells to decrease the expression of FAK. Modified Boyden chambers and MTT assay were used to examine the effect of FAK inhibition on the invasiveness and proliferation of SGC7901. RESULTS: EGF activated FAK(Y397) and p130cas(Y410) phosphorylation, while Fn activated ERK general phosphorylation. Inhibition of FAK expression decreased p130cas(Y410) phosphorylation activated by EGF and ERK general phosphorylation activated by Fn, also decreased the invasiveness and proliferation of SGC7901 cells activated by EGF or Fn. CONCLUSION: There is crosstalk between EGFR and integrin signal transduction. FAK may be a key cross point of the two signal pathways and acts as a potential target for human gastric cancer therapy.
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spelling pubmed-34818562012-10-29 Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901 Dan, Li Jian, Ding Na, Lin Xiaozhong, Wang Onco Targets Ther Original Research BACKGROUND/OBJECTIVE: To investigate the crosstalk between epidermal growth factor receptor (EGFR) and integrin-mediated signal transduction pathways in human gastric adenocarcinoma cells. METHODS: EGF was used as a ligand of EGFR to stimulate the gastric adenocarcinoma cell, SGC7901. Signal molecules downstream of the integrin, FAK(Y397) and p130cas(Y410) phosphorylation, were measured by immunoprecipitation and western blot. Fibronectin (Fn) was used as a ligand of integrin to stimulate the same cell line. Signal molecules downstream of EGFR and extracellular signal-regulated kinase (ERK) general phosphorylation were also measured. Focal adhesion kinase (FAK) small-interfering RNA was designed and transfected into SGC7901 cells to decrease the expression of FAK. Modified Boyden chambers and MTT assay were used to examine the effect of FAK inhibition on the invasiveness and proliferation of SGC7901. RESULTS: EGF activated FAK(Y397) and p130cas(Y410) phosphorylation, while Fn activated ERK general phosphorylation. Inhibition of FAK expression decreased p130cas(Y410) phosphorylation activated by EGF and ERK general phosphorylation activated by Fn, also decreased the invasiveness and proliferation of SGC7901 cells activated by EGF or Fn. CONCLUSION: There is crosstalk between EGFR and integrin signal transduction. FAK may be a key cross point of the two signal pathways and acts as a potential target for human gastric cancer therapy. Dove Medical Press 2012-10-23 /pmc/articles/PMC3481856/ /pubmed/23109808 http://dx.doi.org/10.2147/OTT.S35322 Text en © 2012 Dan et al, publisher and licensee Dove Medical Press Ltd This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.
spellingShingle Original Research
Dan, Li
Jian, Ding
Na, Lin
Xiaozhong, Wang
Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901
title Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901
title_full Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901
title_fullStr Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901
title_full_unstemmed Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901
title_short Crosstalk between EGFR and integrin affects invasion and proliferation of gastric cancer cell line, SGC7901
title_sort crosstalk between egfr and integrin affects invasion and proliferation of gastric cancer cell line, sgc7901
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481856/
https://www.ncbi.nlm.nih.gov/pubmed/23109808
http://dx.doi.org/10.2147/OTT.S35322
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