PERSONAL DE APOYO
CABALLERO Fabiana Alejandra
artículos
Título:
Cell cycle arrest and modulation of HO-1 expression induced by
Autor/es:
P. SACCA; F. CABALLERO; A. BATTLE; E. VAZQUEZ
Revista:
INTERNATIONAL JOURNAL OF BIOCHEMISTRY AND CELLULAR BIOLOGY
Editorial:
ELSEVIER
Referencias:
Año: 2004 vol. 36 p. 1945 - 1953
ISSN:
1357-2725
Resumen:
Abstract
Background and aims: Control of cell proliferation is important for cancer prevention since cell proliferation has an
essential role in carcinogenesis. In rodent carcinogenesis models, antioxidant agents suppress carcinogen-induced cellular
hyper proliferation in the target organs. Strict control of cell division is an essential process to ensure that DNA synthesis and
mitotic division are accurately and coordinately executed.We studied the interplay between cell cycle and heme oxygenase-1
(HO-1) and the effect of the acetylsalicylic acid (ASA) in hepatic carcinogenesis. Methods: Male CF1 mice pre-treated
with dietary p-dimethylaminoazobenzene (DAB; 0.5%, w/w) were fed with ASA (0.16%, w/w). We investigated the hepatic
expression of cyclin D1, cyclin E, Cdk2, Cdk4, p21, p27, p53; the level of bcl-2, an antiapoptotic protein and of heme
oxygenase-1 (HO-1), a marker of oxidative stress, by Western blot analysis. Results: The treatment with ASA produced
an important attenuation in the induction of cyclin E and cyclin D1 provoked by DAB. p21 and p27 levels were increased
when animals received both drugs. The administration of ASA to DAB treated animals induced Cdk2 (29%). HO-1 induction
(65%) provoked by DAB was diminished by ASA administration reaching lower induction levels (23%). Conclusion: The
deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment
of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their
DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.
© 2004 Elsevier Ltd. All rights reserved.Control of cell proliferation is important for cancer prevention since cell proliferation has an
essential role in carcinogenesis. In rodent carcinogenesis models, antioxidant agents suppress carcinogen-induced cellular
hyper proliferation in the target organs. Strict control of cell division is an essential process to ensure that DNA synthesis and
mitotic division are accurately and coordinately executed.We studied the interplay between cell cycle and heme oxygenase-1
(HO-1) and the effect of the acetylsalicylic acid (ASA) in hepatic carcinogenesis. Methods: Male CF1 mice pre-treated
with dietary p-dimethylaminoazobenzene (DAB; 0.5%, w/w) were fed with ASA (0.16%, w/w). We investigated the hepatic
expression of cyclin D1, cyclin E, Cdk2, Cdk4, p21, p27, p53; the level of bcl-2, an antiapoptotic protein and of heme
oxygenase-1 (HO-1), a marker of oxidative stress, by Western blot analysis. Results: The treatment with ASA produced
an important attenuation in the induction of cyclin E and cyclin D1 provoked by DAB. p21 and p27 levels were increased
when animals received both drugs. The administration of ASA to DAB treated animals induced Cdk2 (29%). HO-1 induction
(65%) provoked by DAB was diminished by ASA administration reaching lower induction levels (23%). Conclusion: The
deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment
of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their
DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.
© 2004 Elsevier Ltd. All rights reserved.Methods: Male CF1 mice pre-treated
with dietary p-dimethylaminoazobenzene (DAB; 0.5%, w/w) were fed with ASA (0.16%, w/w). We investigated the hepatic
expression of cyclin D1, cyclin E, Cdk2, Cdk4, p21, p27, p53; the level of bcl-2, an antiapoptotic protein and of heme
oxygenase-1 (HO-1), a marker of oxidative stress, by Western blot analysis. Results: The treatment with ASA produced
an important attenuation in the induction of cyclin E and cyclin D1 provoked by DAB. p21 and p27 levels were increased
when animals received both drugs. The administration of ASA to DAB treated animals induced Cdk2 (29%). HO-1 induction
(65%) provoked by DAB was diminished by ASA administration reaching lower induction levels (23%). Conclusion: The
deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment
of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their
DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.
© 2004 Elsevier Ltd. All rights reserved.p-dimethylaminoazobenzene (DAB; 0.5%, w/w) were fed with ASA (0.16%, w/w). We investigated the hepatic
expression of cyclin D1, cyclin E, Cdk2, Cdk4, p21, p27, p53; the level of bcl-2, an antiapoptotic protein and of heme
oxygenase-1 (HO-1), a marker of oxidative stress, by Western blot analysis. Results: The treatment with ASA produced
an important attenuation in the induction of cyclin E and cyclin D1 provoked by DAB. p21 and p27 levels were increased
when animals received both drugs. The administration of ASA to DAB treated animals induced Cdk2 (29%). HO-1 induction
(65%) provoked by DAB was diminished by ASA administration reaching lower induction levels (23%). Conclusion: The
deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment
of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their
DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.
© 2004 Elsevier Ltd. All rights reserved.Results: The treatment with ASA produced
an important attenuation in the induction of cyclin E and cyclin D1 provoked by DAB. p21 and p27 levels were increased
when animals received both drugs. The administration of ASA to DAB treated animals induced Cdk2 (29%). HO-1 induction
(65%) provoked by DAB was diminished by ASA administration reaching lower induction levels (23%). Conclusion: The
deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment
of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their
DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.
© 2004 Elsevier Ltd. All rights reserved.Conclusion: The
deregulation of cyclin/CDK expression and the up-regulation of p21 and p27 with the administration of ASA, post-treatment
of the carcinogen administration, would block the pass through out to the G0/G1 check point to permit the cells to repair their
DNA and HO-1 protected the liver from reactive oxygen species produced from DAB.
© 2004 Elsevier Ltd. All rights reserved.