Abstract |
Aberrant regulation of histone deacetylase 2 (HDAC2) plays a pivotal role in the development of hepatocellular carcinoma (HCC), but, the underlying mechanism leading to HDAC2 overexpression is not well understood. We performed microRNA ( miRNA) profiling analysis in a subset of HCCs, and identified four down-regulated miRNAs that may target HDAC2 in HCC. Ectopic expression of miRNA mimics evidenced that miR-145 suppresses HDAC2 expression in HCC cells. This treatment repressed cancer cell growth and recapitulated HDAC2 knockdown effects on HCC cells. In conclusion, we suggest that loss or suppression of miR-145 may cause aberrant overexpression of HDAC2 and promote HCC tumorigenesis.
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Authors | Ji Heon Noh, Young Gyoon Chang, Min Gyu Kim, Kwang Hwa Jung, Jeong Kyu Kim, Hyun Jin Bae, Jung Woo Eun, Qingyu Shen, Seung-Jin Kim, So Hee Kwon, Won Sang Park, Jung Young Lee, Suk Woo Nam |
Journal | Cancer letters
(Cancer Lett)
Vol. 335
Issue 2
Pg. 455-62
(Jul 28 2013)
ISSN: 1872-7980 [Electronic] Ireland |
PMID | 23499894
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2013 Elsevier Ireland Ltd. All rights reserved. |
Chemical References |
- MIRN145 microRNA, human
- MicroRNAs
- RNA, Small Interfering
- HDAC2 protein, human
- Histone Deacetylase 2
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Topics |
- Animals
- Carcinoma, Hepatocellular
(genetics)
- Cell Line, Tumor
- Cell Proliferation
- Genes, Tumor Suppressor
- Histone Deacetylase 2
(genetics, metabolism)
- Humans
- Liver Neoplasms
(genetics)
- Mice
- Mice, Nude
- MicroRNAs
(genetics, metabolism)
- Neoplasm Transplantation
- RNA Interference
- RNA, Small Interfering
- Xenograft Model Antitumor Assays
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