Journal List > Korean J Gynecol Oncol Colposc > v.11(1) > 1123649

Moon, Choi, and Park: The expression and tyrosine phosphorylation of E-cadherin, beta-, gamma-catenin and EGFR after treatment of EGF and TGF-alpha in Cervical Cancer Cell Lines

Abstract

OBJECTIVES

Cadherin/catenin adhesion complex is fundamentally involved in epithelial cancer invasion and metastasis. E-cadherin and EGFR colocalize on the basolateral membrane of epithelial cell and EGF down-regulate E-cadherin expression. In the invasion and metastasis of cancer, E-cadherin expression is decreased and growth factors receptor is overexpressed. The present study was aimed to find the role of E-cadherin, beta-and gamma-catenin, growth factors and its receptors in cervical cancer cell lines.

METHODS

The cervical cancer cell cultures were treated with different time duration of EGF 30 ng/ml and TGF-a 10 ng/ml(0, 10 min, 20 min, 30 min, 1 hr, 2 hr, 4 hr, 8 hr, 24 hr). The change in cancer cell morphology and the changes in E-cadherin, beta- and gamma-catenin, EGFR and activated EGFR expression were studied with a western blot analysis and an immunoprecipitation.

RESULTS

Through a western blot analysis, E-cadherin 120 kDa band and EGFR 170 kDa band were expressed in CaSki, HT-3 and ME-180 cell line, which showed epithelial contact growth. 1n these 3 cell lines, expression of E-cadherin did not decrease with time dependent manner. after the treatment of EGF and TGF- alpha. The expression of EGFR decreased and activated EGFR expression increased in 30 minutes to 1 hour but decreased subsequently. When the cells treated with EGF, there were no change in beta-and gamma-catenin expression with there dependent manner. The tyrosine phosphorylation of beta-and gamma-catenin increased in 30 minutes to 1 hour but decreased subsequently with activated EGFR.

CONCLUSION

This study showed that an activated EGFR which has involved with tyrosine phosphorylation of beta- and gamma-catenin influenced by growth factors rather than expression of E-cadherin, has a role in the invasion and metastasis of the cervical cancer.

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