The correlation of IL-8 signaling pathway and EGFR pathway in MDA-231 cells of breast carcinoma
- VernacularTitle:乳腺癌MDA-231细胞中IL-8与表皮生长因子受体信号通路的关系
- Author:
Tianying ZHENG
;
Yonggang WANG
;
Xin ZHANG
;
Xueqin GAO
;
Huaning ZHANG
- Publication Type:Journal Article
- Keywords:
Interleukin-8;
Epidermal growth factor receptor(EGFR);
G protein-coupled receptor(GPCR):Transactivation;
Breast carcinoma
- From:
Chinese Journal of Microbiology and Immunology
2008;28(4):303-307
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of IL-8 on cell proliferation and invasion,and to analyze the correlations between chemokine and epidermal growth factor receptor(EGFR)signaling pathways in breast carcinoma cells.Methods IL-8 secretion responded to treatment with rhEGF and anti-EGFR and expression of its receptors CXCR1,CXCR2 in MDA-231 cells were measured by ELISA and immunocytochemistry,respectively.Effect of rhIL-8 and neutralizing antibody on cell proliferation and invasion were analyzed by using MTT and matrigel invasion assay.EGFR transactivation stimulated with rhIL-8 and neutralizing an tibody was assessed by Western blot using anti-phosphotyrosine antibody.Results MDA-231 cells released hish level of IL-8 and two receptom of IL-8(CXCR1 and CXCR2)both expressed on cell membrane.Exogenous IL-8 and its neutralizing antibody did not significantly influence the proliferation of breast carcinoma cells,but rhIL-8 stimulated invasive activity in MDA-231 cells and its neutralizing antibody inhibited the in vasive activity(P<0.05).EGF and anti-EGFR both inhibited the secretion of IL-8 in breast carcinoma cells,and IL-8 had no effect on EGFR phosphorylation,but anti-IL-8 induced transactivation of EGFR after 24h.Conclusion IL-8 contributes to tumor progression in breast carcinoma through its enhancement of in vasive activitv but not act as an autocrine growth factor.The correlation of competitive inhibition rather than cross-talk is found between G protein coupled receptor(GPCR)-mediated IL-8 signaling pathway and EGFR pathway in breast carcinoma.