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.
They called me mad, and I called them mad,
and damn them, they outvoted me.