In an upcoming G&D paper, Dr. Albert Baldwin and colleagues (UNC School of Medicine) lend new insight into an alternate mechanism of p53 inactivation in tumor cells. The researchers found that the putative oncoprotein Bcl-3, which is expressed in some leukemias and solid tumors, potently suppresses p53 activation through a mechanism that involves the controlled upregulation of Hdm2 gene expression.
Additionally, they found that Bcl-3 is activated by DNA damage and is required for p53 to control Hdm2 gene expression. Thus the normal function of Bcl-3 appears to be to limit p53 activation and to suppress apoptosis. Constitutive expression of Bcl-3 in cancer, therefore, subverts the normal regulation of the p53 tumor suppressor mechanism leading to oncogenic potential.
Heather Cosel | EurekAlert!
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