Journal
CLINICAL EPIGENETICS
Volume 8, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/s13148-016-0208-3
Keywords
Hepatocellular carcinoma; DNA methylation; Q-MSP; PAX6; HCV
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Funding
- Ministry of Science and Technology, Taiwan [MOST 104-2314-B-016-047, MOST 104-2321-B-016-003, MOST 103-2314-B-016-008]
- Ministry of National Defense, Taiwan [MAB-104-004, MAB-104-005, MAB-104-006, MAB-105-001, MAB-105-002, MAB-105-003]
- Liver Disease Prevention and Treatment Research Foundation, Taiwan, Republic of China
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Background: Related to genetic alteration, frequent promoter hypermethylation is also a contributing factor in the development of human cancers. Recently, we discovered numerous novel genes that were aberrantly methylated in hepatocellular carcinoma (HCC) by using Infinium HumanMethylation27 BeadChip array. We utilized a quantitative methylation-specific PCR (Q-MSP) system for the evaluation of PAX6 methylation in 29 normal controls and 160 paired HCC tissues and their adjacent non-tumor tissues. We verified the correlation between the methylation status of PAX6 and clinical characteristics with different viral status. Results: Paired-box 6 promoter methylation was observed in 39.4 %, 15.6 %, and 3.4 % in primary HCCs, adjacent nontumors, and normal control tissues, respectively. Methylation of the PAX6 promoter region in HCCs significantly increased compared with control tissues. PAX6 was frequently methylated in HCV-positive HCC tissues (61.3 %) and rarely methylated in HBV-positive (22.1 %) and double-negative HCC tissues (33.3 %). Conclusions: Our data suggests that promoter hypermethylation of PAX6 is a common event in HCCs and the association of PAX6 methylation in clinicopathological features is divergent with different viral status.
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