J Korean Med Sci.
2006 Oct;21(5):891-896. 10.3346/jkms.2006.21.5.891.
Expression of the RERG Gene is Gender-Dependent in Hepatocellular Carcinoma and Regulated by Histone Deacetyltransferases
- Affiliations
-
- 1Laboratory of Human Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea. dslee@kangwon.ac.kr
- 2Department of Internal Medicine, Kangnam St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea.
- 3Laboratory of Molecular Oncology, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
- 4Depatment of Surgery, School of Medicine Ajou University, Suwon, Korea.
- 5Department of Pathology, College of Medicine, Chungnam National University, Daejeon, Korea.
- 6Department of Surgery, SUN General Hospital, Daejeon, Korea.
- 7Animal Resources Science, Kangwon National University, Chuncheon, Korea.
- KMID: 1781911
- DOI: http://doi.org/10.3346/jkms.2006.21.5.891
Abstract
- Ras-related, estrogen-regulated, and growth-inhibitory gene (RERG) is a novel gene that was first reported in breast cancer. However, the functions of RERG are largely unknown in other tumor types. In this study, RERG expression was analyzed in hepatocellular carcinomas of human patients using reverse transcriptase PCR analysis. In addition, the possible regulation of RERG expression by histone deacetyltransferases (HDACs) was studied in several cell lines. Interestingly, the expression of RERG gene was increased in hepatocellular carcinoma (HCC) of male patients (57.9%) but decreased in HCC of females (87.5%) comparison with paired peri-tumoral tissues. Moreover, RERG gene expression was increased in murine hepatoma Hepa1-6 cells, human breast tumor MDA-MB-231 cells, and mouse normal fibroblast NIH3T3 cells after treated by HDAC inhibitor, trichostatin A. Our results suggest that RERG may function in a gender-dependent manner in hepatic tumorigenesis and that the expression of this gene may be regulated by an HDAC-related signaling pathway.
Keyword
MeSH Terms
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Signal Transduction
Sex Factors
Mice, Transgenic
Mice, Inbred C57BL
Mice
Male
Liver Neoplasms/*genetics
Humans
Histone Deacetylases/*physiology
Hepatocytes/metabolism
Growth Inhibitors/*genetics
*Genes, ras
*Gene Expression Regulation, Neoplastic
Female
Estrogens/*pharmacology
Estrogen Receptor alpha/analysis
Cell Proliferation
Animals
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