Journal
CANCER LETTERS
Volume 329, Issue 2, Pages 164-173Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2012.10.027
Keywords
Hepatocellular carcinoma; 5-Aza-2 '-deoxycytidine; Trichostatin A; Cell proliferation; G2/M arrest
Categories
Funding
- China National Key Projects for Infectious Disease [2012ZX10002012-008]
- Chinese National Key Program on Basic Research [2010CB529204, 2012CB22308]
- National Natural Science Foundation [81071722, 81201690]
Ask authors/readers for more resources
Growing evidence indicates that some tumor suppressive miRNAs are subject to epigenetic modifications during carcinogenesis. Here, we found that a large miRNA cluster of C19MC was upregulated in HCC cells after combined treatment with DNA methylation inhibitor and histone deacetylase inhibitor. MiR-517a and miR-517c were strikingly different from the remaining 41 miRNAs in C19MC. Ectopic expression of MiR-517a and miR-517c inhibited cell proliferation by blocking G2/M transition, whereas down-regulation of miR-517a and miR-517c facilitated cell growth. We further showed Pyk2 is a target of miR-517a and miR-517c and both the miRNAs are downregulated in HCC samples. These data collectively suggest that down-regulation of both miR-517a and miR-517c contribute to HCC development through regulating Pyk2. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available