Carcinogenesis, Vol 19, 2001-2006, Copyright © 1998 by Oxford University Press
QS Wang, A Papanikolaou, CL Sabourin and DW Rosenberg
Alterations in the expression of the cell cycle regulators, cyclin D1 and
cyclin-dependent kinase 4 (Cdk4), have been implicated in malignancies of
both humans and experimental animal models. We hypothesize that altered
expression of cyclin D1 and Cdk4 may also be involved in mouse colon
tumorigenesis induced by the chemical carcinogen, azoxymethane (AOM). In
the present study, SWR/J mice were given AOM by i.p. injection at a dose of
10 mg/kg once a week for 8 weeks, and colonic tissue and tumors were
isolated 18 weeks later. The expression and localization of cyclin D1 and
Cdk4 were examined by reverse transcription-polymerase chain reaction
(RT-PCR) and immunohistochemical analyses. Cyclin D1 and Cdk4 mRNA levels
in tumor samples were increased 1.3-fold (P < 0.01) and 1.2-fold (P <
0.01), respectively, when compared with control mouse colon tissue. Control
colon epithelium was uniformly negative for cyclin D1 immunoreactivity,
whereas minimal Cdk4 nuclear staining was confined to the lower portion of
the crypts within the control tissue. Both cyclin D1 and Cdk4
immunoreactive cells were markedly increased in preneoplastic lesions and
in adenomas isolated from AOM-treated mice. Furthermore, some
morphologically normal colon crypts from AOM-treated mice showed positive
cyclin D1 immunoreactivity. These findings suggest that overexpression of
cyclin D1 and Cdk4 occurs early in the AOM-induced mouse colon
tumorigenesis and may contribute to tumor progression in this model.
ARTICLES
Altered expression of cyclin D1 and cyclin-dependent kinase 4 in azoxymethane-induced mouse colon tumorigenesis
University of Connecticut School of Pharmacy, Department of Pharmaceutical Sciences, Storrs 06269-2091, USA.
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