Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis.

Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis. Research Abstract Details 

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Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis. Abstract Text:

Jennifer M Phillips,Yukio Yamamoto,Masahiko Negishi,Robert R Maronpot,Jay I Goodman,

Altered DNA methylation is an epigenetic mechanism that plays a key role in the carcinogenesis process, and the nongenotoxic rodent hepatocarcinogen phenobarbital (PB) alters the methylation status of DNA in mouse liver. The constitutive active/androstane nuclear receptor (CAR) mediates half of the PB-induced hepatic gene expression changes and it is essential for liver tumor promotion in PB-treated mice. Here, a technique involving methylation-sensitive restriction digestion, arbitrarily primed PCR, and capillary electrophoresis was utilized to detect PB-induced regions of altered DNA methylation (RAMs) in CAR wildtype (WT) mice that are sensitive to promotion by PB and resistant CAR knockout (KO) mice. The CAR WT mice developed preneoplastic lesions after 23 weeks of PB treatment (precancerous) and liver tumors after 32 weeks, while the CAR KO mice did not develop tumors (Y. Yamamoto, et al., 2004, Cancer Res. 64, 7197-7200). Our goal was to discern those RAMs which are playing important roles in tumor formation by comparing the RAMs that form in sensitive and resistant groups of mice. Using this novel approach, 42 unique RAMs were identified in the precancerous as compared to the CAR KO, 23-week PB-treated tissue. Of these 42 RAMs, 14 carried forward to the tumor tissue, and additionally, 104 total unique RAMs were observed in the tumor tissue. These results indicate that there are unique RAMs occurring in the sensitive CAR WT mice and that a portion of these are seen in both the precancerous and tumor tissue. We hypothesize that these unique RAMs may be facilitating the tumorigenesis process, and these data support the view that DNA methylation plays a causative role in PB-induced tumorigenesis.

Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis. Publishing Authors By Initials

JM Phillips,Y Yamamoto,M Negishi,RR Maronpot,JI Goodman,

For similar proteins: transcription factors research abstracts see: proteins: transcription factors research

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Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Toxicological sciences : an official journal of th

VOLUME: 96

Page Numbers: 72-82

Journal Abbreviation: Toxicol. Sci.

ISSN: 1096-6080

DAY: 16

MONTH: 12

YEAR: 2006

Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 9805461

Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis. Keywords Mesh Terms:

KEYWORDS: Transcription Factors

MESH TERMS: metabolism

Chemical & Substance for Abstract: Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis. Information

Substance Name: Diethylnitrosamine

Registry Number: 55-18-5

Grant and Affiliation Information for Orphan nuclear receptor constitutive active/androstane receptor-mediated alterations in DNA methylation during phenobarbital promotion of liver tumorigenesis.

AFFILIATION: Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824, USA.

Country: United States

AGENCY: United States NIEHS

GRANT: T32-ES-7255

ACRONYM: ES

MEDLINETA: Toxicol Sci

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