Epigenetics of hepatocellular carcinoma: Role of microRNA

被引:63
作者
Khare, Sharad [1 ,2 ]
Zhang, Qiong [1 ]
Ibdah, Jamal A. [1 ]
机构
[1] Univ Missouri, Div Gastroenterol & Hepatol, Dept Internal Med, Columbia, MO 65212 USA
[2] Harry S Truman Mem Vet Hosp, Columbia, MO 65201 USA
关键词
MicroRNA; Cancer; Hepatocellular carcinoma; Biomarker; Polymorphism; SUPPRESSES CELL-PROLIFERATION; DOWN-REGULATION CONTRIBUTES; LIVER-CANCER; GROWTH-FACTOR; UP-REGULATION; INSERTION/DELETION POLYMORPHISM; MESENCHYMAL TRANSITION; INHIBITS PROLIFERATION; HEPATOCARCINOMA CELLS; UNTRANSLATED REGION;
D O I
10.3748/wjg.v19.i33.5439
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Hepatocellular carcinoma (HCC) represents a major form of primary liver cancer in adults. MicroRNAs (miRs), small non-coding single-stranded RNAs of 19-24 nucleotides in length, negatively regulate the expression of many target genes at the post-transcriptional and/or translational levels and play a critical role in the initiation and progression of HCC. In this review we have summarized the information of aberrantly expressed miRs in HCC, their mechanism of action and relationship to cancer. The recent advances in HCC research reveal that miRs regulate expression of various oncogenes and tumor suppressor genes, thereby contributing to the modulation of diverse biological processes including proliferation, apoptosis, epithelial to mesenchymal transition and metastasis. From a clinical viewpoint, polymorphisms within miR-binding sites are associated with the risk of HCC. Polymorphisms in miR related genes have been shown to correlate with survival or treatment outcome in patients. Furthermore, the review focuses on the potential role of miRs as novel biomarkers and their translational applications for diagnosis and therapy in HCC. With further insights into miR deregulation in HCC, it is expected that novel miR-based therapeutics will arise. Also, we orient the readers to other reviews that may provide better understanding of miR research in HCC. (C) 2013 Baishideng. All rights reserved.
引用
收藏
页码:5439 / 5445
页数:7
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