Artículos de revistas
Single CpG island methylation is not sufficient to maintain the silenced expression of CASPASE-8 apoptosis-related gene among women with epithelial ovarian cancer
Fecha
2014-02-01Registro en:
Biomedicine & Pharmacotherapy. Paris: Elsevier France-editions Scientifiques Medicales Elsevier, v. 68, n. 1, p. 87-91, 2014.
0753-3322
10.1016/j.biopha.2013.12.004
WOS:000332448400014
8334785337106990
Autor
Diretoria Pesquisa & Desenvolvimento Fdn Ezequiel
Universidade Federal de Minas Gerais (UFMG)
Universidade Estadual Paulista (Unesp)
Institución
Resumen
Despite impressive research efforts, the biology of epithelial ovarian cancer (EOC) remains poorly understood and alterations in the expression of CASPASE-8 contribute to a worse tumor prognosis. This study assesses the methylation of the CpG island within the CASPASE-8 promoter and CASPASE-8 gene expression both in cystadenoma tumors and in primary and metastatic EOC. DNA and RNA were obtained from women with normal ovarian tissues (n = 18), ovarian serous cystadenoma tumors (n = 11) and EOC (n = 16) using Trizol (R). The methylation frequency of the CpG island in the CASPASE-8 promoter was assessed using the methylation-specific PCR assay after DNA bisulfite conversion. Quantitative PCR was performed to quantify the relative levels of CASPASE-8 in each sample. The differences between samples with each group were evaluated using the Mann-Whitney U and Kruskal-Wallis tests as indicated. Hemimethylation of the CASPASE-8 promoter was found in 11.8% of the normal ovary samples, 20% of the cystadenoma tumors and 20% of the metastatic EOC, while methylation of the CASPASE-8 promoter was absent in the EOC primary tissues (P = 0.047). An increased CASPASE-8 expression level was observed in all tumor groups. Significant differences were observed in the CASPASE-8 expression levels when compared with all ovarian tumor groups (P = 0.0278). Promoter DNA methylation did not associate with expression levels of CASPASE-8, suggesting the presence of other mechanisms in relation to gene expression control in EOC; thus providing a better understanding of this complex disease. (C) 2013 Elsevier Masson SAS. All rights reserved.