Title:
Epigenetic changes within the promoter region of the HLA-G gene in ovarian tumors

Thumbnail Image
Author(s)
Menendez, Laura
Walker, L. DeEtte
Matyunina, Lilya V.
Totten, Kimberly A.
Benigno, Benedict B.
McDonald, John F.
Authors
Advisor(s)
Advisor(s)
Editor(s)
Associated Organization(s)
Organizational Unit
Organizational Unit
School of Biological Sciences
School established in 2016 with the merger of the Schools of Applied Physiology and Biology
Series
Supplementary to
Abstract
Background: Previous findings have suggested that epigenetic-mediated HLA-G expression in tumor cells may be associated with resistance to host immunosurveillance. To explore the potential role of DNA methylation on HLA-G expression in ovarian cancer, we correlated differences in HLA-G expression with methylation changes within the HLA-G regulatory region in an ovarian cancer cell line treated with 5-aza-deoxycytidine (5-aza-dC) and in malignant and benign ovarian tumor samples and ovarian surface epithelial cells (OSE) isolated from patients with normal ovaries. Results: A region containing an intact hypoxia response element (HRE) remained completely methylated in the cell line after treatment with 5-aza-dC and was completely methylated in all of the ovarian tumor (malignant and benign) samples examined, but only variably methylated in normal OSE samples. HLA-G expression was significantly increased in the 5-aza-dC treated cell line but no significant difference was detected between the tumor and OSE samples examined. Conclusion: Since HRE is the binding site of a known repressor of HLA-G expression (HIF-1), we hypothesize that methylation of the region surrounding the HRE may help maintain the potential for expression of HLA-G in ovarian tumors. The fact that no correlation exists between methylation and HLA-G gene expression between ovarian tumor samples and OSE, suggests that changes in methylation may be necessary but not sufficient for HLA-G expression in ovarian cancer.
Sponsor
Date Issued
2008-05-22
Extent
Resource Type
Text
Resource Subtype
Article
Rights Statement
Rights URI