| First Author | Kimura S | Year | 2012 |
| Journal | Mol Cancer | Volume | 11 |
| Pages | 90 | PubMed ID | 23234329 |
| Mgi Jnum | J:316964 | Mgi Id | MGI:6843308 |
| Doi | 10.1186/1476-4598-11-90 | Citation | Kimura S, et al. (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. Mol Cancer 11:90 |
| abstractText | BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: The DNA binding of C/EBP family members can be used as a potential molecular target for lung cancer therapy. |
