Tyrosine phosphorylation of 尾-catenin affects its subcellular localization and transcriptional activity of 尾-catenin in Hela and Bcap-37 cells

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• 作者：He-Ya Qian^a ; Ding-Guo Zhang^a ; Hong-Wei Wang^a ; Dong-Sheng Pei^a ; ^{dspei@xzmc.edu.cn" class="auth_mail} ; Jun-Nian Zheng^a ; ^b ; ^{jnzheng@xzmc.edu.cn" class="auth_mail}
• 关键词：Tyrosine phosphorylation ; 尾-Catenin ; Genistein ; Ki-67
• 刊名：Bioorganic and Medicinal Chemistry Letters
• 出版年：1 June 2014
• 年：2014
• 卷：24
• 期：11
• 页码：2565-2570
• 全文大小：1104 K

文摘

In order to investigate the relationship between tyrosine phosphorylation of 尾-catenin and transcriptional activity of 尾-catenin in Hela and Bcap-37 cells, genistein (a tyrosine kinase inhibitor) was used to inhibit tyrosine phosphorylation in cells. Our results showed the total 尾-catenin protein levels were mainly equal in Hela, Bcap-37 and HK-2 cells, 尾-catenin was mainly present in nucleus in Hela and Bcap-37cells, while in HK-2 cell 尾-catenin was mainly located in cytoplasm. Genistein could inhibit tyrosine phosphorylation of 尾-catenin and downregulate nuclear 尾-catenin expression in Hela and Bcap-37 cells. In addition, genistein suppressed Ki-67 promoter activity and Ki-67 protein level, thus promoted cell apoptosis. Furthermore, 尾-catenin could increase the Ki-67 promoter activity in Hela and Bcap-37 cells. From these findings we conclude that tyrosine phosphorylation of 尾-catenin can regulate the cellular distribution of 尾-catenin and affect the transcriptional activity of 尾-catenin.