TNFR1 promoter -329G/T polymorphism results in allele-specific repression of TNFR1 expression

Sun Kim; Song Mean Moon; Yong Sung Kim; Jae Jung Kim; Ha Jung Ryu; Yeon Jung Kim; Jung Won Choi; Hong Seok Park; Dae Ghon Kim; Hyoung Doo Shin; Mark S. Rutherford; Bermseok Oh; Jong Keuk Lee

doi:10.1016/j.bbrc.2008.01.098

TNFR1 promoter -329G/T polymorphism results in allele-specific repression of TNFR1 expression

Sun Kim, Song Mean Moon, Yong Sung Kim, Jae Jung Kim, Ha Jung Ryu, Yeon Jung Kim, Jung Won Choi, Hong Seok Park, Dae Ghon Kim, Hyoung Doo Shin, Mark S. Rutherford, Bermseok Oh, Jong Keuk Lee

Veterinary and Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

Abstract

Tumor necrosis factor (TNF) and the TNF receptor (TNFR) superfamily play very important roles for cell death as well as normal immune regulation. Dysregulation of TNF-TNFR superfamily gene expression will influence many biological processes, and contributes to human diseases, including cancer. We investigated the genetic alterations of the TNF-TNFR superfamily genes in hepatocellular carcinoma (HCC). Several genetic alterations were detected in the 44 TNF-TNFR superfamily genes by sequencing hepatocellular carcinoma DNA samples. In particular, we found that the TNFR1 promoter -329G/T polymorphism was strongly associated with primary HCC (odds ratio [OR] = 5.22, p = 0.0007). We also observed frequent loss of heterozygosity at the polymorphic TNFR1 -329G/T site in the primary tumor tissues, indicating that the polymorphic TNFR1 -329G/T site is very susceptible to genetic alterations in HCC. Furthermore, in the polymorphic TNFR1 -329G/T site, the T allele resulted in the repression of TNFR1 expression. Therefore, our results suggest that TNFR1 -329G/T polymorphism may play an important role in the development of HCC.

Original language	English (US)
Pages (from-to)	395-401
Number of pages	7
Journal	Biochemical and Biophysical Research Communications
Volume	368
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2008.01.098
State	Published - Apr 4 2008

Bibliographical note

Funding Information:
The authors are grateful to Dr. A. Fujiyama (RIKEN Genomic Sciences Center, Japan) for the provision of sample supplies (chimpanzee DNA). This work was supported in part by a Grant (#0720200) of the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea and a Grant (#07-419) from the Asan Institute for Life Sciences, Seoul, Korea.

Keywords

Hepatocellular carcinoma
Promoter
Single nucleotide polymorphism (SNP)
TNFR1

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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Kim, S., Moon, S. M., Kim, Y. S., Kim, J. J., Ryu, H. J., Kim, Y. J., Choi, J. W., Park, H. S., Kim, D. G., Shin, H. D., Rutherford, M. S., Oh, B., & Lee, J. K. (2008). TNFR1 promoter -329G/T polymorphism results in allele-specific repression of TNFR1 expression. Biochemical and Biophysical Research Communications, 368(2), 395-401. https://doi.org/10.1016/j.bbrc.2008.01.098

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title = "TNFR1 promoter -329G/T polymorphism results in allele-specific repression of TNFR1 expression",

abstract = "Tumor necrosis factor (TNF) and the TNF receptor (TNFR) superfamily play very important roles for cell death as well as normal immune regulation. Dysregulation of TNF-TNFR superfamily gene expression will influence many biological processes, and contributes to human diseases, including cancer. We investigated the genetic alterations of the TNF-TNFR superfamily genes in hepatocellular carcinoma (HCC). Several genetic alterations were detected in the 44 TNF-TNFR superfamily genes by sequencing hepatocellular carcinoma DNA samples. In particular, we found that the TNFR1 promoter -329G/T polymorphism was strongly associated with primary HCC (odds ratio [OR] = 5.22, p = 0.0007). We also observed frequent loss of heterozygosity at the polymorphic TNFR1 -329G/T site in the primary tumor tissues, indicating that the polymorphic TNFR1 -329G/T site is very susceptible to genetic alterations in HCC. Furthermore, in the polymorphic TNFR1 -329G/T site, the T allele resulted in the repression of TNFR1 expression. Therefore, our results suggest that TNFR1 -329G/T polymorphism may play an important role in the development of HCC.",

keywords = "Hepatocellular carcinoma, Promoter, Single nucleotide polymorphism (SNP), TNFR1",

author = "Sun Kim and Moon, {Song Mean} and Kim, {Yong Sung} and Kim, {Jae Jung} and Ryu, {Ha Jung} and Kim, {Yeon Jung} and Choi, {Jung Won} and Park, {Hong Seok} and Kim, {Dae Ghon} and Shin, {Hyoung Doo} and Rutherford, {Mark S.} and Bermseok Oh and Lee, {Jong Keuk}",

note = "Funding Information: The authors are grateful to Dr. A. Fujiyama (RIKEN Genomic Sciences Center, Japan) for the provision of sample supplies (chimpanzee DNA). This work was supported in part by a Grant (#0720200) of the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea and a Grant (#07-419) from the Asan Institute for Life Sciences, Seoul, Korea.",

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AU - Kim, Sun

AU - Moon, Song Mean

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AU - Kim, Jae Jung

AU - Ryu, Ha Jung

AU - Kim, Yeon Jung

AU - Choi, Jung Won

AU - Park, Hong Seok

AU - Kim, Dae Ghon

AU - Shin, Hyoung Doo

AU - Rutherford, Mark S.

AU - Oh, Bermseok

AU - Lee, Jong Keuk

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PY - 2008/4/4

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N2 - Tumor necrosis factor (TNF) and the TNF receptor (TNFR) superfamily play very important roles for cell death as well as normal immune regulation. Dysregulation of TNF-TNFR superfamily gene expression will influence many biological processes, and contributes to human diseases, including cancer. We investigated the genetic alterations of the TNF-TNFR superfamily genes in hepatocellular carcinoma (HCC). Several genetic alterations were detected in the 44 TNF-TNFR superfamily genes by sequencing hepatocellular carcinoma DNA samples. In particular, we found that the TNFR1 promoter -329G/T polymorphism was strongly associated with primary HCC (odds ratio [OR] = 5.22, p = 0.0007). We also observed frequent loss of heterozygosity at the polymorphic TNFR1 -329G/T site in the primary tumor tissues, indicating that the polymorphic TNFR1 -329G/T site is very susceptible to genetic alterations in HCC. Furthermore, in the polymorphic TNFR1 -329G/T site, the T allele resulted in the repression of TNFR1 expression. Therefore, our results suggest that TNFR1 -329G/T polymorphism may play an important role in the development of HCC.

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KW - Single nucleotide polymorphism (SNP)

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TNFR1 promoter -329G/T polymorphism results in allele-specific repression of TNFR1 expression

Abstract

Bibliographical note

Keywords

UN SDGs

Access

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