Journal
MOLECULAR CANCER
Volume 9, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1476-4598-9-223
Keywords
-
Categories
Funding
- Consejo Nacional de Ciencia y Tecnologia [C01-45728]
Ask authors/readers for more resources
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
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available