A tumor suppressor role for C/EBPα in solid tumors: More than fat and blood

A. R. Lourenço, P. J. Coffer*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

1 Citation (Scopus)


The transcription factor CCAAT/enhancer-binding protein alpha (C/EBPα) 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/EBPα. Deregulation of C/EBPα 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/EBPα function in non-hematopoietic tissues is regulated by alternative mechanisms. Here we review the function of C/EBPα in solid tumors and focus on the molecular mechanisms underlying its tumor suppressive role.

Original languageEnglish
Pages (from-to)5221-5230
Number of pages10
Issue number37
Publication statusPublished - 14 Sept 2017


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