Suppression of extracellular signals and cell proliferation through EGF receptor binding by (-)-epigallocatechin gallate in human A431 epidermoid carcinoma cells

Yu Chih Liang, Shoei Yn Lin-shiau, Chieh Fu Chen, Jen Kun Lin

研究成果: 雜誌貢獻文章

273 引文 斯高帕斯(Scopus)

摘要

Tea polyphenols are known to inhibit a wide variety of enzymatic activities associated with cell proliferation and tumor progression. The molecular mechanisms of antiproliferation are remained to be elucidated. In this study, we investigated the effects of the major tea polyphenol (-)- epigallocatechin gallate (EGCG) on the proliferation of human epidermoid carcinoma cell line, A431. Using a [3H]thymidine incorporation assay, EGCG could significantly inhibit the DNA synthesis of A431 cells. In vitro assay, EGCG strongly inhibited the protein tyrosine kinase (PTK) activities of EGF- R, PDGF-R, and FGF-R, and exhibited an IC50 value of 0.5-1 μg/ml. But EGCG scarcely inhibited the protein kinase activities of pp60(v-src), PKC, and PKA (IC50 > 10 μg/ml). In an in vivo assay, EGCG could reduce the autophosphorylation level of EGF-R by EGR. Phosphoamino acid analysis of the EGF-R revealed that EGCG inhibited the EGF-stimulated increase in phosphotyrosine level in A431 cells. In addition, we showed that EGCG blocked EGF binding to its receptor. The results of further studies suggested that the inhibition of proliferation and suppression of the EGF signaling by EGCG might mainly mediate dose-dependent blocking of ligand binding to its receptor, and subsequently through inhibition of EGF-R kinase activity.
原文英語
頁(從 - 到)55-65
頁數11
期刊Journal of Cellular Biochemistry
67
發行號1
DOIs
出版狀態已發佈 - 十月 1 1997
對外發佈Yes

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

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