TY - JOUR
T1 - A tumor suppressor role for C/EBPα in solid tumors
T2 - More than fat and blood
AU - Lourenço, A. R.
AU - Coffer, P. J.
N1 - Publisher Copyright:
© 2017 Macmillan Publishers Limited, part of Springer Nature. All rights reserved.
PY - 2017/9/14
Y1 - 2017/9/14
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85031695785&partnerID=8YFLogxK
U2 - 10.1038/onc.2017.151
DO - 10.1038/onc.2017.151
M3 - Review article
C2 - 28504718
SN - 0950-9232
VL - 36
SP - 5221
EP - 5230
JO - Oncogene
JF - Oncogene
IS - 37
ER -