Format

Send to

Choose Destination
Mol Cancer. 2010 Aug 24;9:223. doi: 10.1186/1476-4598-9-223.

Depletion of the oncoprotein Bcl-3 induces centrosome amplification and aneuploidy in cancer cells.

Author information

1
Biotechnology Unit, Grupo Farmacéutico Neolpharma, Mexico City, Mexico.

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.

PMID:
20731879
PMCID:
PMC2933622
DOI:
10.1186/1476-4598-9-223
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center