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.
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| http://dx.doi.org/10.1186/1476-4598-7-43 | DOI Listing |
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Article Synopsis
- Hepatitis C (HCV) in people who are also infected with HIV leads to faster liver disease progression compared to those with only HCV, potentially due to HLA-G, which suppresses immune responses.
- A study analyzed liver samples from 59 patients with both chronic HCV and HIV to look at HLA-G levels in relation to liver disease severity.
- The results showed that higher HLA-G expression was linked to more severe liver conditions but did not affect the effectiveness of HCV treatment, indicating HLA-G's complex role in disease progression in coinfected patients.
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