| First Author | Lourenço AR | Year | 2017 |
| Journal | Oncogene | Volume | 36 |
| Issue | 37 | Pages | 5221-5230 |
| PubMed ID | 28504718 | Mgi Jnum | J:248093 |
| Mgi Id | MGI:5926894 | Doi | 10.1038/onc.2017.151 |
| Citation | Lourenco AR, et al. (2017) A tumor suppressor role for C/EBPalpha in solid tumors: more than fat and blood. Oncogene 36(37):5221-5230 |
| abstractText | The transcription factor CCAAT/enhancer-binding protein alpha (C/EBPalpha) plays a critical role during embryogenesis and is thereafter required for homeostatic glucose metabolism, adipogenesis and myeloid development. Its ability to regulate the expression of lineage-specific genes and induce growth arrest contributes to the terminal differentiation of several cell types, including hepatocytes, adipocytes and granulocytes. CEBPA loss of-function mutations contribute to the development of ~10% of acute myeloid leukemia (AML), stablishing a tumor suppressor role for C/EBPalpha. Deregulation of C/EBPalpha expression has also been reported in a variety of additional human neoplasias, including liver, breast and lung cancer. However, functional CEBPA mutations have not been found in solid tumors, suggesting that abrogation of C/EBPalpha function in non-hematopoietic tissues is regulated by alternative mechanisms. Here we review the function of C/EBPalpha in solid tumors and focus on the molecular mechanisms underlying its tumor suppressive role. |
