| First Author | Cai Y | Year | 2015 |
| Journal | PLoS One | Volume | 10 |
| Issue | 3 | Pages | e0120647 |
| PubMed ID | 25767874 | Mgi Jnum | J:232975 |
| Mgi Id | MGI:5780527 | Doi | 10.1371/journal.pone.0120647 |
| Citation | Cai Y, et al. (2015) CCAAT/enhancer binding protein beta is dispensable for development of lung adenocarcinoma. PLoS One 10(3):e0120647 |
| abstractText | Lung cancer is the leading cause of cancer death worldwide. Although disruption of normal proliferation and differentiation is a vital component of tumorigenesis, the mechanisms of this process in lung cancer are still unclear. A transcription factor, C/EBPbeta is a critical regulator of proliferation and/or differentiation in multiple tissues. In lung, C/EBPbeta is expressed in alveolar pneumocytes and bronchial epithelial cells; however, its roles on normal lung homeostasis and lung cancer development have not been well described. Here we investigated whether C/EBPbeta is required for normal lung development and whether its aberrant expression and/or activity contribute to lung tumorigenesis. We showed that C/EBPbeta was expressed in both human normal pneumocytes and lung adenocarcinoma cell lines. We found that overall lung architecture was maintained in Cebpb knockout mice. Neither overexpression of nuclear C/EBPbeta nor suppression of CEBPB expression had significant effects on cell proliferation. C/EBPbeta expression and activity remained unchanged upon EGF stimulation. Furthermore, deletion of Cebpb had no impact on lung tumor burden in a lung specific, conditional mutant EGFR lung cancer mouse model. Analyses of data from The Cancer Genome Atlas (TCGA) revealed that expression, promoter methylation, or copy number of CEBPB was not significantly altered in human lung adenocarcinoma. Taken together, our data suggest that C/EBPbeta is dispensable for development of lung adenocarcinoma. |
