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Expression of the RERG gene is gender-dependent in hepatocellular carcinoma and regulated by histone deacetyltransferases.

Wang AG, Fang W, Han YH, Cho SM, Choi JY, Lee KH, Kim WH, Kim JM, Park MG, Yu DY, Kim NS, Lee DS - J. Korean Med. Sci. (2006)

Bottom Line: Ras-related, estrogen-regulated, and growth-inhibitory gene (RERG) is a novel gene that was first reported in breast cancer.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.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Human Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea.

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.

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RERG expression in trichostatin A (TSA)-treated cells. Expression of the gene was analyzed by RT-PCR. NIH3T3, MDA-MD0-231, and Hepa1-6 cells were treated with 0.5 µM or 1 µm of the histone deacetyltransferases (HDAC) inhibitor TSA. GAPDH was used as a quantitative control. M, size marker.
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Figure 5: RERG expression in trichostatin A (TSA)-treated cells. Expression of the gene was analyzed by RT-PCR. NIH3T3, MDA-MD0-231, and Hepa1-6 cells were treated with 0.5 µM or 1 µm of the histone deacetyltransferases (HDAC) inhibitor TSA. GAPDH was used as a quantitative control. M, size marker.

Mentions: HDACs are important in proliferation diseases, owing largely to the functions of these enzymes in regulating gene expression (8). It was therefore of interest to determine whether the RERG gene is under the regulation of HDACs. Several cell lines were treated with the HDAC inhibitor TSA, and RERG expression was subsequently analyzed by RT-PCR. The results show that RERG expression was regulated by HDACs in NIH3T3, MDA-MB-231, and Hepa1-6 cells (Fig. 5). We therefore propose that RERG plays an important role in the inhibition of cell proliferation in several tumor cell types, as has been reported in vitro and in vivo in breast cancer cells.


Expression of the RERG gene is gender-dependent in hepatocellular carcinoma and regulated by histone deacetyltransferases.

Wang AG, Fang W, Han YH, Cho SM, Choi JY, Lee KH, Kim WH, Kim JM, Park MG, Yu DY, Kim NS, Lee DS - J. Korean Med. Sci. (2006)

RERG expression in trichostatin A (TSA)-treated cells. Expression of the gene was analyzed by RT-PCR. NIH3T3, MDA-MD0-231, and Hepa1-6 cells were treated with 0.5 µM or 1 µm of the histone deacetyltransferases (HDAC) inhibitor TSA. GAPDH was used as a quantitative control. M, size marker.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2722001&req=5

Figure 5: RERG expression in trichostatin A (TSA)-treated cells. Expression of the gene was analyzed by RT-PCR. NIH3T3, MDA-MD0-231, and Hepa1-6 cells were treated with 0.5 µM or 1 µm of the histone deacetyltransferases (HDAC) inhibitor TSA. GAPDH was used as a quantitative control. M, size marker.
Mentions: HDACs are important in proliferation diseases, owing largely to the functions of these enzymes in regulating gene expression (8). It was therefore of interest to determine whether the RERG gene is under the regulation of HDACs. Several cell lines were treated with the HDAC inhibitor TSA, and RERG expression was subsequently analyzed by RT-PCR. The results show that RERG expression was regulated by HDACs in NIH3T3, MDA-MB-231, and Hepa1-6 cells (Fig. 5). We therefore propose that RERG plays an important role in the inhibition of cell proliferation in several tumor cell types, as has been reported in vitro and in vivo in breast cancer cells.

Bottom Line: Ras-related, estrogen-regulated, and growth-inhibitory gene (RERG) is a novel gene that was first reported in breast cancer.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.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.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Human Genomics, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea.

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.

Show MeSH
Related in: MedlinePlus