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01.12.2012 | Research | Ausgabe 1/2012 Open Access

Molecular Cancer 1/2012

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 > Ausgabe 1/2012
Shioko Kimura, Jorge Paiz, Mitsuhiro Yoneda, Taketomo Kido, Charles Vinson, Jerrold M Ward
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1476-4598-11-90) contains supplementary material, which is available to authorized users.

Competing interests

All authors declare that they do not have any competing interests.

Authors’ contribution

SK designed the study, partiscipated in carcinogenesis experiments, analyzed the data, preparing the figures and tables, and wrote a paper. JP and TK carried out carcinogenesis experiments, and prepared histological samples. MY prepared histological samples and performed immunohistochemistry. CV participated in designing carcinogenesis experiments, data analysis and interpretation of the results. JMW participated in designing carcinogenesis study, examined histological specimens, and analyzed the data and helped preparing the tables. All authors read and approved the final manuscript.



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.


A transgenic mouse line expressing a dominant negative A-C/EBP under the promoter of lung epithelial Clara cell secretory protein (CCSP) 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.


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.


The DNA binding of C/EBP family members can be used as a potential molecular target for lung cancer therapy.
Authors’ original file for figure 1
Authors’ original file for figure 2
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