Epigenetic and expression analysis of TRAIL-R2 and BCL2: on the TRAIL to knowledge of apoptosis in ovarian tumors
Objective This study assesses TRAIL - R2 ( TNF-related apoptosis-inducing ligand receptor 2) and BCL2 (B cell CLL/lymphoma 2) expression as well as CpG island methylation within the TRAIL - R2 promoter in ovarian serous tumors and primary and metastatic serous EOC (epithelial ovarian cancer). Method...
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Veröffentlicht in: | Archives of gynecology and obstetrics 2014-05, Vol.289 (5), p.1061-1069 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Objective
This study assesses
TRAIL
-
R2 (
TNF-related apoptosis-inducing ligand receptor 2) and
BCL2
(B cell CLL/lymphoma 2) expression as well as CpG island methylation within the
TRAIL
-
R2
promoter in ovarian serous tumors and primary and metastatic serous EOC (epithelial ovarian cancer).
Methods
RNA and DNA were obtained from women with normal ovarian tissues (
n
= 18), ovarian serous cystadenoma tumors (
n
= 11) and serous EOC (
n
= 16) using Trizol
®
. Quantitative PCR was performed to quantify the relative levels of
TRAIL
-
R2
and
BCL2
. The methylation frequency of the
TRAIL
-
R3
promoter was assessed using a methylation-specific PCR assay after DNA bisulfite conversion. Differences between the groups were evaluated using the
χ
2
, Mann–Whitney
U
or Kruskal–Wallis tests, as indicated.
Results
We identified
TRAIL
-
R2
and
BCL2
mRNA expressed in all ovarian tumor groups, and there were significant differences between the groups. Both genes had low expression levels in ovarian serous cystadenoma and primary EOC tumors when compared with metastatic EOC. Methylation of the
TRAIL
-
R2
promoter was frequently observed in all groups; however, there were no statistically significant associations.
Conclusions
Primary EOC is associated with lower
TRAIL
-
R2
and
BCL2
expression levels, while metastatic EOC is associated with higher expression of these genes. Promoter DNA methylation was not related to this finding, suggesting there are other mechanisms involved in transcriptional control. |
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ISSN: | 0932-0067 1432-0711 |
DOI: | 10.1007/s00404-013-3060-0 |