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Abstract
Bcl-3 is an atypical member of the inhibitor of NF-kappa B family of proteins since it can function as a coactivator of transcription. Although this oncogene was described in leukemia, it is overexpressed in a number of solid tumors as well. The oncogenic potential of Bcl-3 has been associated with its capacity to increase proliferation by means of activating the cyclin D1 promoter and to its antiapoptotic role mediated by the inhibiton of p53 activity. In the course of dissecting these properties, we found that depleting Bcl-3 protein using shRNAs induce a decrease of proliferation and clonogenic survival associated with the induction of multinucleation and increased ploidy. These effects were associated with a DNA damage response, a delay in G2/M checkpoint and the induction of centrosome amplification
Highlights
Bcl-3 is an atypical member of the inhibitor of NF-kappa B family of proteins since it can function as a coactivator of transcription
The Bcl-3 oncogene was first identified in a subset of patients with chronic lymphocytic leukemia (CLL) in the region adjacent to the t(14;19)(q32;q13) translocation [1,2]
While Bcl-3 overexpression was originally found to be associated with CLL and lymphomas, recent reports have shown that this oncogene is overexpressed
Summary
Bcl-3 is an atypical member of the inhibitor of NF-kappa B family of proteins since it can function as a coactivator of transcription. An additional role for Bcl-3 in carcinogenesis has recently been suggested by Kashatus et al, who demonstrated that after DNA damage, Bcl-3 is required for the induction of Hdm2 gene expression and the suppression of persistent p53 activity [12]. These results suggest that the oncogenic role of Bcl-3 could be mediated by a p53-dependent pathway, possibly by preventing the apoptosis of cells with damaged DNA.
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