Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouse

<p>Abstract</p> <p>Background</p> <p>The CCAAT/enhancer binding proteins (C/EBPs) play important roles in carcinogenesis of many tumors including the lung. Since multiple C/EBPs are expressed in lung, the combinatorial expression of these C/EBPs on lung carcinogenesis i...

Full description

Bibliographic Details
Main Authors: Kimura Shioko, Paiz Jorge, Yoneda Mitsuhiro, Kido Taketomo, Vinson Charles, Ward Jerrold M
Format: Article
Language:English
Published: BMC 2012-12-01
Series:Molecular Cancer
Subjects:
Online Access:http://www.molecular-cancer.com/content/11/1/90
_version_ 1811249475047391232
author Kimura Shioko
Paiz Jorge
Yoneda Mitsuhiro
Kido Taketomo
Vinson Charles
Ward Jerrold M
author_facet Kimura Shioko
Paiz Jorge
Yoneda Mitsuhiro
Kido Taketomo
Vinson Charles
Ward Jerrold M
author_sort Kimura Shioko
collection DOAJ
description <p>Abstract</p> <p>Background</p> <p>The CCAAT/enhancer binding proteins (C/EBPs) play important roles in carcinogenesis of many tumors including the lung. Since multiple C/EBPs are expressed in lung, the combinatorial expression of these C/EBPs on lung carcinogenesis is not known.</p> <p>Methods</p> <p>A transgenic mouse line expressing a dominant negative A-C/EBP under the promoter of lung epithelial Clara cell secretory protein (<it>CCSP</it>) gene in doxycycline dependent fashion was subjected to 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung carcinogenesis bioassay in the presence and absence of doxycycline, and the effect of abolition of DNA binding activities of C/EBPs on lung carcinogenesis was examined.</p> <p>Results</p> <p>A-C/EBP expression was found not to interfere with tumor development; however, it suppressed the malignant conversion of adenoma to carcinoma during NNK-induced lung carcinogenesis. The results suggested that Ki67 may be used as a marker for lung carcinomas in mouse.</p> <p>Conclusions</p> <p>The DNA binding of C/EBP family members can be used as a potential molecular target for lung cancer therapy.</p>
first_indexed 2024-04-12T15:48:13Z
format Article
id doaj.art-0f93e89eee4547aebbf90d2e5e4378f1
institution Directory Open Access Journal
issn 1476-4598
language English
last_indexed 2024-04-12T15:48:13Z
publishDate 2012-12-01
publisher BMC
record_format Article
series Molecular Cancer
spelling doaj.art-0f93e89eee4547aebbf90d2e5e4378f12022-12-22T03:26:36ZengBMCMolecular Cancer1476-45982012-12-011119010.1186/1476-4598-11-90Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouseKimura ShiokoPaiz JorgeYoneda MitsuhiroKido TaketomoVinson CharlesWard Jerrold M<p>Abstract</p> <p>Background</p> <p>The CCAAT/enhancer binding proteins (C/EBPs) play important roles in carcinogenesis of many tumors including the lung. Since multiple C/EBPs are expressed in lung, the combinatorial expression of these C/EBPs on lung carcinogenesis is not known.</p> <p>Methods</p> <p>A transgenic mouse line expressing a dominant negative A-C/EBP under the promoter of lung epithelial Clara cell secretory protein (<it>CCSP</it>) gene in doxycycline dependent fashion was subjected to 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung carcinogenesis bioassay in the presence and absence of doxycycline, and the effect of abolition of DNA binding activities of C/EBPs on lung carcinogenesis was examined.</p> <p>Results</p> <p>A-C/EBP expression was found not to interfere with tumor development; however, it suppressed the malignant conversion of adenoma to carcinoma during NNK-induced lung carcinogenesis. The results suggested that Ki67 may be used as a marker for lung carcinomas in mouse.</p> <p>Conclusions</p> <p>The DNA binding of C/EBP family members can be used as a potential molecular target for lung cancer therapy.</p>http://www.molecular-cancer.com/content/11/1/90C/EBPsLung chemical carcinogenesis bioassayDominant negativeA-C/EBPTransgenic mouse4-(methylnitrosamino)-1-(3-pyridyl)-1-butanoneNNK
spellingShingle Kimura Shioko
Paiz Jorge
Yoneda Mitsuhiro
Kido Taketomo
Vinson Charles
Ward Jerrold M
Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouse
Molecular Cancer
C/EBPs
Lung chemical carcinogenesis bioassay
Dominant negative
A-C/EBP
Transgenic mouse
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
NNK
title Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouse
title_full Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouse
title_fullStr Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouse
title_full_unstemmed Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouse
title_short Deficiency of CCAAT/enhancer binding protein family DNA binding prevents malignant conversion of adenoma to carcinoma in NNK-induced lung carcinogenesis in the mouse
title_sort deficiency of ccaat enhancer binding protein family dna binding prevents malignant conversion of adenoma to carcinoma in nnk induced lung carcinogenesis in the mouse
topic C/EBPs
Lung chemical carcinogenesis bioassay
Dominant negative
A-C/EBP
Transgenic mouse
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone
NNK
url http://www.molecular-cancer.com/content/11/1/90
work_keys_str_mv AT kimurashioko deficiencyofccaatenhancerbindingproteinfamilydnabindingpreventsmalignantconversionofadenomatocarcinomainnnkinducedlungcarcinogenesisinthemouse
AT paizjorge deficiencyofccaatenhancerbindingproteinfamilydnabindingpreventsmalignantconversionofadenomatocarcinomainnnkinducedlungcarcinogenesisinthemouse
AT yonedamitsuhiro deficiencyofccaatenhancerbindingproteinfamilydnabindingpreventsmalignantconversionofadenomatocarcinomainnnkinducedlungcarcinogenesisinthemouse
AT kidotaketomo deficiencyofccaatenhancerbindingproteinfamilydnabindingpreventsmalignantconversionofadenomatocarcinomainnnkinducedlungcarcinogenesisinthemouse
AT vinsoncharles deficiencyofccaatenhancerbindingproteinfamilydnabindingpreventsmalignantconversionofadenomatocarcinomainnnkinducedlungcarcinogenesisinthemouse
AT wardjerroldm deficiencyofccaatenhancerbindingproteinfamilydnabindingpreventsmalignantconversionofadenomatocarcinomainnnkinducedlungcarcinogenesisinthemouse