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Carcinogenesis Advance Access published online on November 4, 2005
Carcinogenesis, doi:10.1093/carcin/bgi261
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received May 10, 2005
Revised October 13, 2005
Accepted October 30, 2005

CANCER BIOLOGY

Novel retinoblastoma binding protein RBBP9 modulates sex-specific radiation responses in vivo

Scott Cassie 1 #, Igor Koturbash 1 #, Darryl Hudson 1, Mike Baker 1, Yaroslav Ilnytskyy 1, Rocio Rodriguez-Juarez 1, Edgar Weber 2, and Olga Kovalchuk 1*

1 Department of Biological Sciences, University of Lethbridge, Lethbridge, Alberta, T1K 3M4, Canada
2 DSM Nutritional Products Ltd, Kaiseraugst, CH-4303, Switzerland

* To whom correspondence should be addressed.
Olga Kovalchuk, E-mail: olga.kovalchuk{at}uleth.ca


  Abstract

Retinoblastoma tumor suppressor (RB) is a key regulator of apoptosis, a central mediator of the proliferative block induced by ionizing radiation (IR) and a binding target for a variety of proteins that regulate its activity (1). One of the recently discovered and the least investigated of these is the novel Rb-binding protein RBBP9/BOG (2). We studied the effects of acute and chronic low dose radiation (LDR) exposure on the induction of RBBP9 and RB signaling pathway in vivo in mouse spleen and found that RBBP9 played a pivotal role in IR responses in vivo. We observed that chronic LDR exposure led to a significant increase of RBBP9 expression in males and a significant decrease in females. Elevated RBBP9 expression in males was paralleled by a pronounced dephosphorylation of RB and a significant drop of PCNA and cyclin A expression. On the contrary, chronic exposure in females led to decreased levels of RBBP9 and increased levels of hyperphosphorylated RB (ppRB) in spleen. Decreased levels of ppRB in spleen of chronically exposed males were correlated with strongly elevated apoptotic rates. In females, the radiation-induced increase of apoptotic index was much less pronounced.

Quite surprisingly, the observed sex-specific signaling changes did not result in the sex-specificity of cellular proliferation. The molecular mechanisms and possible repercussions of the radiation-induced sex differences in cellular proliferation and apoptosis are discussed.

# - two authors contributed equally to the research, there names are listed in alphabetical order
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