Publication: Cooperative role between p21cip1/waf1
and p27kip1 in premature senescence
in glandular proliferative lesions in mice
Authors
García-Fernández, R.A. ; García-Palencia, P. ; Suárez, C. ; Sánchez, M.A. ; Gil-Gómez, G. ; Sánchez, B. ; Rollán, E. ; Martín-Caballero, J. ; Flores, J.M.
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Cellular senescence has been considered a
novel target for cancer therapy. It has also been pointed
out that p21cip1/waf1 and p27kip1 cyclin-dependent kinase
inhibitors (CKIs) play a role in cellular senescence in
some tumor types. Therefore, in order to address the
possibility of a cooperative role between p21 and p27
proteins in senescence in vivo we analyzed cellular
senescence in spontaneous glandular proliferative
lesions (adrenal, thyroid and pituitary glands) in a
double-KO mice model, using γH2AX, p53, p16, PTEN
and Ki67 as senescence markers. The results obtained
showed that p21p27 double-null mice had the lowest
number of γH2AX positive cells in glandular
hyperplasias and benign tumors. Also, in this group,
Ki67 proliferation index correlated with a lower
immunohistochemical expression of γH2AX and p53.
The expression of p16 and PTEN do not seem to cause
synergism of senescence in the benign lesions analyzed
in p21p27 double-KO mice. These observations suggest
an intrinsic cooperation between p21 and p27 CKIs in
the activation of stress-induced cellular senescence and
tumor progression in vivo, which would be a
physiological mechanism to prevent tumor cell
proliferation.
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Citation
Histology and Histopathology, vol. 29, nº 3 (2014)
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