The Bcl-w promoter is activated by beta-catenin/TCF4 in human colorectal carcinoma cells

Gene
Abigail LaphamGraham Packham

Abstract

The antiapoptotic BCL-2 family protein BCL-W is often overexpressed in colorectal carcinoma (CRC) where it correlates with advanced stage and expression of p53. In this work we have analysed the Bcl-w promoter to identify potential regulators of BCL-W expression in CRC cells. The Bcl-w promoter was highly active in cell lines derived from CRC as well as other cancer types. Although expression of p53 and BCL-W correlate in CRC, overexpression of wild type or mutant p53 did not significantly alter Bcl-w promoter activity, and deletion of endogenous p53 did not alter the expression of Bcl-w RNA in HCT116 cells. Promoter deletion analysis lead to the identification of a potential binding site for TCF/LEF factors, obligate binding partners for beta-catenin, a downstream target of the WNT signalling pathway. TCF4 and beta-catenin interacted with the Bcl-w promoter in intact HCT116 cells and mutation of this site significantly decreased promoter activity. The activity of the Bcl-w promoter was increased or decreased, respectively, by overexpression of beta-catenin or dominant negative TCF4. beta-catenin is activated in the majority of CRC and these results suggest that BCL-W may function as a downstream effector of inappropriate WNT/b...Continue Reading

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Citations

Mar 6, 2010·Journal of Cancer Research and Clinical Oncology·Wallace Martins de AraújoJose Andres Morgado-Diaz
Apr 14, 2009·Trends in Molecular Medicine·Shi Yu YangMarc C Winslet
Apr 2, 2015·Biochimica Et Biophysica Acta·Cristina CorreiaScott H Kaufmann
Jan 24, 2019·Frontiers in Oncology·Clare M AdamsChristine M Eischen
Apr 23, 2020·Cell Death & Disease·Mariusz L Hartman, Malgorzata Czyz
Apr 15, 2021·Future Medicinal Chemistry·Hao ZhangQingwei Zhang

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