PMID- 15751032
OWN - NLM
STAT- MEDLINE
DCOM- 20050721
LR  - 20231213
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 115
IP  - 6
DP  - 2005 Jul 20
TI  - Effect of the tumor promoter phenobarbital on the pattern of global gene 
      expression in liver of connexin32-wild-type and connexin32-deficient mice.
PG  - 861-9
AB  - The antiepileptic drug phenobarbital (PB) is used frequently as a model tumor 
      promoter in rodent liver. It is believed to increase the probability of cancer by 
      accelerating the clonal expansion of cells transformed during tumor initiation. 
      The molecular mechanism underlying this process is only partly understood but 
      seems to require the function of connexin32 (Cx32), one of the 2 gap junction 
      proteins expressed in hepatocytes. PB mediates transcriptional activation of 
      various genes in liver but which of these are relevant for tumor promotion is 
      unknown. We have used oligonucleotide microarrays to identify genes 
      differentially modulated in expression by PB in liver of Cx32-wild-type and 
      Cx32-null mice. Mice of both strains were kept on PB containing (0.05%) or 
      control diet for 2 weeks. Total liver RNA was isolated from 3 mice per 
      experimental group and reverse transcribed; cDNAs were hybridized to 
      oligonucleotide microarrays and a gene-by-gene linear model was used for 
      statistical analysis of data. Five genes were identified as induced or repressed 
      in untreated Cx32-null as compared to untreated Cx32-wild-type mice. PB affected 
      the expression of 53 genes, of which 13 code for members of Phase-I/II of drug 
      metabolism, and 12 genes were differentially affected in expression by PB in 
      Cx32-null as compared to Cx32-wild-type mice. Among the differentially affected 
      genes that could be verified by quantitative RT-PCR or Western analysis were the 
      insulin like growth factor binding protein-1, retinol dehydrogenase-6 and the 
      Y-chromosomally located gene Dby, among which may be a candidate of relevance for 
      PB-mediated tumor promotion.
CI  - Copyright 2005 Wiley-Liss, Inc.
FAU - Stahl, Sabine
AU  - Stahl S
AD  - Institut fur Pharmakologie und Toxikologie, Abteilung Toxikologie, Universitat 
      Tubingen, Germany.
FAU - Ittrich, Carina
AU  - Ittrich C
FAU - Marx-Stoelting, Philip
AU  - Marx-Stoelting P
FAU - Kohle, Christoph
AU  - Kohle C
FAU - Ott, Thomas
AU  - Ott T
FAU - Buchmann, Albrecht
AU  - Buchmann A
FAU - Schwarz, Michael
AU  - Schwarz M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (Carcinogens)
RN  - 0 (Connexins)
RN  - YQE403BP4D (Phenobarbital)
SB  - IM
MH  - Animals
MH  - Carcinogens/*pharmacology
MH  - Connexins/*genetics
MH  - Female
MH  - Gene Expression/drug effects
MH  - Gene Expression Profiling
MH  - Liver/*drug effects
MH  - Male
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Oligonucleotide Array Sequence Analysis
MH  - Phenobarbital/*pharmacology
MH  - Gap Junction beta-1 Protein
EDAT- 2005/03/08 09:00
MHDA- 2005/07/22 09:00
CRDT- 2005/03/08 09:00
PHST- 2005/03/08 09:00 [pubmed]
PHST- 2005/07/22 09:00 [medline]
PHST- 2005/03/08 09:00 [entrez]
AID - 10.1002/ijc.20815 [doi]
PST - ppublish
SO  - Int J Cancer. 2005 Jul 20;115(6):861-9. doi: 10.1002/ijc.20815.