Methylation alterations are not a major cause of PTTG1 missregulation

Thumbnail
View/Open
Issue date
2008
Author
Hidalgo, Manuel
Galan, Jose J.
Sáez, Carmen
Ferrero, Eduardo
Castilla, Carolina
Ramirez Lorca, Reposo
Pelaez, Pablo
Ruiz, Agustín
Japón, Miguel A.
Royo Sánchez-Palencia, José Luis
Suggested citation
Hidalgo, Manuel; Galan, Jose J.; Sáez, Carmen; Ferrero, Eduardo; Castilla, Carolina; Ramirez Lorca, Reposo; ... Royo Sánchez-Palencia, José Luis. (2008) . Methylation alterations are not a major cause of PTTG1 missregulation. BMC Cancer, 2008, vol. 8, núm. 110, p. 1-9. https://doi.org/10.1186/1471-2407-8-110.
Impact

Google Scholar logo  Google Scholar
Share
Export to Mendeley
Metadata
Show full item record
Abstract
Background: 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.
URI
http://hdl.handle.net/10459.1/60018
DOI
https://doi.org/10.1186/1471-2407-8-110
Is part of
BMC Cancer, 2008, vol. 8, núm. 110, p. 1-9
Collections

The following license files are associated with this item:

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