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Cooperative role between p21cip1/waf1 and p27kip1 in premature senescence in glandular proliferative lesions in mice

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dc.contributor.authorGarcía-Fernández, R.A.
dc.contributor.authorGarcía-Palencia, P.
dc.contributor.authorSuárez, C.
dc.contributor.authorSánchez, M.A.
dc.contributor.authorGil-Gómez, G.
dc.contributor.authorSánchez, B.
dc.contributor.authorRollán, E.
dc.contributor.authorMartín-Caballero, J.
dc.contributor.authorFlores, J.M.
dc.date.accessioned2019-02-05T15:19:32Z
dc.date.available2019-02-05T15:19:32Z
dc.date.issued2014
dc.description.abstractCellular 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.es
dc.formatapplication/pdfes
dc.format.extent10es
dc.identifier.citationHistology and Histopathology, vol. 29, nº 3 (2014)
dc.identifier.issn1699-5848
dc.identifier.issn0213-3911
dc.identifier.urihttp://hdl.handle.net/10201/67240
dc.languageenges
dc.publisherF. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histologíaes
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectAnimal modeles
dc.subjectHyperplasiaes
dc.subject.otherCDU::5 - Ciencias puras y naturales::57 - Biología::576 - Biología celular y subcelular. Citologíaes
dc.titleCooperative role between p21cip1/waf1 and p27kip1 in premature senescence in glandular proliferative lesions in micees
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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Histology and histopathology Vol.29, nº 3 (2014)