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

Molecular Cancer

Short Communication

Ruben Zamora¹  Magali Espinosa²  Gisela Ceballos-Cancino²  Jorge Melendez-Zajgla³  Blanca Segura⁴  Vilma Maldonado⁵ 

[1] Biotechnology Unit, Grupo Farmacéutico Neolpharma, (Boulevard de los Ferrocarriles 277), (02300), Mexico City, Mexico;Molecular Biology Laboratory, Instituto Nacional de Cancerologia, (Av. San Fernando 22), (14080), Mexico City, Mexico;Cancer Functional Genomics Laboratory, National Institute of Genomic Medicine, (Periferico Sur 4124), (01900), Mexico City, Mexico;Cancer Functional Genomics Laboratory, National Institute of Genomic Medicine, (Periferico Sur 4124), (01900), Mexico City, Mexico;Molecular Biology Laboratory, Instituto Nacional de Cancerologia, (Av. San Fernando 22), (14080), Mexico City, Mexico;Gene Therapy Laboratory, Laboratorios Alpharma, (Renato Leduc 363), (14050), Mexico City, Mexico;Molecular Biology Laboratory, Instituto Nacional de Cancerologia, (Av. San Fernando 22), (14080), Mexico City, Mexico;Molecular Biology Laboratory, Instituto Nacional de Cancerologia, (Av. San Fernando 22), (14080), Mexico City, Mexico;

关键词: Chronic Lymphocytic Leukemia;    Spindle Assembly Checkpoint;    Clonogenic Survival;    Centrosome Amplification;    Centrosome Number;   

DOI  :  10.1186/1476-4598-9-223

 received in 2009-07-20, accepted in 2010-08-24,  发布年份 2010

来源: Springer

【 摘 要 】

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

【 授权许可】

Unknown   
© Zamora et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.