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Oncogene 2013 Aug 15;32(33):3857-66

The tumor suppressor Caliban regulates DNA damage-induced apoptosis through p53-dependent and -independent activity.

Wang Y, Wang Z, Joshi BH, Puri RK, Stultz B, Yuan Q, Bai Y, Zhou P, Yuan Z, Hursh DA, Bi X

Abstract

We previously identified Caliban (Clbn) as the Drosophila homolog of human Serologically defined colon cancer antigen 1 gene and demonstrated that it could function as a tumor suppressor in human non-small-cell lung cancer (NSCLC) cells, although its mode of action was unknown. Herein, we identify roles for Clbn in DNA damage response. We generate clbn knockout flies using homologous recombination and demonstrate that they have a heightened sensitivity to irradiation. We show that normal Clbn function facilitates both p53-dependent and -independent DNA damage-induced apoptosis. Clbn coordinates different apoptosis pathways, showing a two-stage upregulation following DNA damage. Clbn has proapoptotic functions, working with both caspase and the proapoptotic gene Hid. Finally, ecotopic expression of clbn(+) in NSCLC cells suppresses tumor formation in athymic nude mice. We conclude that Caliban is a regulator of DNA damage-induced apoptosis, functioning as a tumor suppressor in both p53-dependent and -independent pathways.Oncogene advance online publication, 10 September 2012; doi:10.1038/onc.2012.395.


Category: Journal Article
PubMed ID: #22964637 DOI: 10.1038/onc.2012.395
Includes FDA Authors from Scientific Area(s): Biologics
Entry Created: 2012-10-17 Entry Last Modified: 2013-09-08
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