Journal
GENE
Volume 543, Issue 1, Pages 101-107Publisher
ELSEVIER
DOI: 10.1016/j.gene.2014.03.059
Keywords
miR-34a; miR-34b/c; Methylation; Hepatocellular carcinoma
Categories
Funding
- National Key Basic Research Program Grant [2013CB911400]
- National Science Foundation for Distinguished Young Scholars of China [81225020]
- Foundation of Jiangsu Province for Distinguished Young Scholars [BK2012042]
- Foundation for the Program for New Century Excellent Talents in University [NCET-10-0178]
- Organization Department of the CPC Central Committee, the Author of National Excellent Doctoral Dissertation [201081]
- National Science Fund for Creative Research Groups [30921006]
- China Postdoctoral Science Foundation [2013M541563]
- Peak of Six Personnel Foundation in Jiangsu Province [WSW-009]
- Jiangsu Province Clinical Science and Technology Projects [BL2012008]
- Priority Academic Program for the Development of Jiangsu Higher Education Institutions
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MicroRNAs (miRNAs) can act as oncogenes or tumor-suppressor genes in human cancers including HCC. Previous studies have identified miR-34 family as an important component of the tumor suppressor network during carcinogenesis. In this study, we investigated the methylation status of miR-34 family in HCC tumor and adjacent non-tumor tissues using methylation-specific PCR (MSP). The methylation frequencies of miR-34a and miR-34b/c were 72.1% (31/43) and 79.1% (34/43) in HCC tissues, which were significantly higher than that in the adjacent non-tumor tissues (P < 0.05), respectively. The results were validated by bisulfite sequencing PCR (BSP). Quantitative reverse transcription polymerase chain reaction (RT-PCR) analysis showed that the expression of miR-34a and miR-34b was significantly down-regulated in HCC tissues compared with adjacent non-tumor tissues (P < 0.05). Moreover, the expression of miR-34b was inversely correlated to CpG island methylation in tumor tissues, but not for miR-34a. In summary, our results suggest that DNA methylation may be involved in the inactivation of miR-34b in HCC. (C) 2014 Elsevier B.V. All rights reserved.
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