Please use this identifier to cite or link to this item: https://doi.org/10.1089/omi.2010.0098
Title: Global Regulation on microRNA in Hepatitis B Virus-Associated Hepatocellular Carcinoma
Authors: Liu, A.M. 
Zhang, C.
Burchard, J.
Fan, S.T.
Wong, K.-F. 
Dai, H.
Poon, R.T.
Luk, J.M.
Issue Date: 1-Mar-2011
Citation: Liu, A.M., Zhang, C., Burchard, J., Fan, S.T., Wong, K.-F., Dai, H., Poon, R.T., Luk, J.M. (2011-03-01). Global Regulation on microRNA in Hepatitis B Virus-Associated Hepatocellular Carcinoma. OMICS A Journal of Integrative Biology 15 (3) : 187-191. ScholarBank@NUS Repository. https://doi.org/10.1089/omi.2010.0098
Abstract: Recent work has revealed the causative links between deregulation of microRNAs (miRNAs) and cancer development. In hepatocellular carcinoma (HCC), aberrant expression of miRNAs has been observed, but the molecular mechanisms that contribute to such changes remains to be elucidated. Here, we reported the analysis of miRNA expression in 94 pairs of tumor and adjacent nontumor tissues from HBV-associated HCC in Chinese patients. We found miRNAs were aberrantly expressed in HCC tissues. To investigate the cause of such deregulation, we detected changes in DNA copy number by measuring locus-specific hybridization intensity, and found changes in expression of several miRNAs are correlated with genomic amplification or deletion. For example, the genomic regions of miR-30d and miR-151 were amplified in ∼50% of HCC tumor tissues, and the expressions of these miRNAs are significantly correlated with DNA copy number. We also employed cDNA microarray data, and provide evidence that key regulators of the miRNA biosynthetic pathway, including DROSHA, DGCR8, AGO1, and AGO2, are frequently overexpressed in HCC. This study provides molecular clues that may contribute to the global changes of miRNA expression in HCC. Copyright © 2011, Mary Ann Liebert, Inc.
Source Title: OMICS A Journal of Integrative Biology
URI: http://scholarbank.nus.edu.sg/handle/10635/110743
ISSN: 15362310
DOI: 10.1089/omi.2010.0098
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