Show simple item record

dc.contributor.authorHidalgo, Manuel
dc.contributor.authorGalan, Jose J.
dc.contributor.authorSáez, Carmen
dc.contributor.authorFerrero, Eduardo
dc.contributor.authorCastilla, Carolina
dc.contributor.authorRamirez Lorca, Reposo
dc.contributor.authorPelaez, Pablo
dc.contributor.authorRuiz, Agustín
dc.contributor.authorJapón, Miguel A.
dc.contributor.authorRoyo Sánchez-Palencia, José Luis
dc.date.accessioned2017-07-10T08:50:40Z
dc.date.available2017-07-10T08:50:40Z
dc.date.issued2008
dc.identifier.issn1471-2458
dc.identifier.urihttp://hdl.handle.net/10459.1/60018
dc.description.abstractBackground: On its physiological cellular context, PTTG1 controls sister chromatid segregation during mitosis. Within its crosstalk to the cellular arrest machinery, relies a checkpoint of integrity for which gained the over name of securin. PTTG1 was found to promote malignant transformation in 3T3 fibroblasts, and further found to be overexpressed in different tumor types. More recently, PTTG1 has been also related to different processes such as DNA repair and found to trans-activate different cellular pathways involving c-myc, bax or p53, among others. PTTG1 over-expression has been correlated to a worse prognosis in thyroid, lung, colorectal cancer patients, and it can not be excluded that this effect may also occur in other tumor types. Despite the clinical relevance and the increasing molecular characterization of PTTG1, the reason for its up-regulation remains unclear. Method: We analysed PTTG1 differential expression in PC-3, DU-145 and LNCaP tumor cell lines, cultured in the presence of the methyl-transferase inhibitor 5-Aza-2'-deoxycytidine. We also tested whether the CpG island mapping PTTG1 proximal promoter evidenced a differential methylation pattern in differentiated thyroid cancer biopsies concordant to their PTTG1 immunohistochemistry status. Finally, we performed whole-genome LOH studies using Affymetix 50 K microarray technology and FRET analysis to search for allelic imbalances comprising the PTTG1 locus. Conclusion: Our data suggest that neither methylation alterations nor LOH are involved in PTTG1 over-expression. These data, together with those previously reported, point towards a post-transcriptional level of missregulation associated to PTTG1 over-expression.ca_ES
dc.description.sponsorshipThis project was funded by The Fundación de Investigación Biomédica Mutua Madrileña Automovilista. Neocodex have been partially funded by the Ministerio de Educación y Ciencia of Spain (FIT-010000-2004-69, PTQ04-1-0006, PTQ2003-0549, PTQ2003-0546 and PTQ2003-0783). MAJ was also supported by SAF2005- 07713-C03-03 and CS by FIS 06/757.ca_ES
dc.language.isoengca_ES
dc.publisherBioMed Centralca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1186/1471-2407-8-110ca_ES
dc.relation.ispartofBMC Cancer, 2008, vol. 8, núm. 110, p. 1-9ca_ES
dc.rightscc-by (c) Hidalgo et al., 2008ca_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleMethylation alterations are not a major cause of PTTG1 missregulationca_ES
dc.typearticleca_ES
dc.identifier.idgrec019954
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1186/1471-2407-8-110


Files in this item

Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record

cc-by (c) Hidalgo et al.,  2008
Except where otherwise noted, this item's license is described as cc-by (c) Hidalgo et al., 2008