Methylation alterations are not a major cause of PTTG1 missregulation

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2008Author
Hidalgo, Manuel
Galan, Jose J.
Sáez, Carmen
Ferrero, Eduardo
Castilla, Carolina
Ramirez Lorca, Reposo
Pelaez, Pablo
Ruiz, Agustín
Japón, Miguel A.
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.
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Show full item recordAbstract
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.
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BMC Cancer, 2008, vol. 8, núm. 110, p. 1-9European research projects
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