Oncogenic role for Bcl-3
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.
By John M. Grohol, Psy.D. on
21 Feb 2009
Published on PsychCentral.com. All rights reserved.
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