PUBLICATION
Non-steady-state hematopoiesis regulated by the C/EBPβ transcription factor
- Authors
- Hirai, H., Yokota, A., Tamura, A., Sato, A., Maekawa, T.
- ID
- ZDB-PUB-150506-6
- Date
- 2015
- Source
- Cancer science 106(7): 797-802 (Review)
- Registered Authors
- Sato, Atsushi
- Keywords
- C/EBPβ, cancer, emergency, hematological malignancy, steady-state
- MeSH Terms
-
- Animals
- CCAAT-Enhancer-Binding Protein-beta/physiology*
- Gene Expression Regulation, Leukemic
- Hematopoiesis*
- Humans
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics
- Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism
- Neutropenia/congenital
- Neutropenia/genetics
- Neutropenia/metabolism
- PubMed
- 25940801 Full text @ Cancer Sci.
Citation
Hirai, H., Yokota, A., Tamura, A., Sato, A., Maekawa, T. (2015) Non-steady-state hematopoiesis regulated by the C/EBPβ transcription factor. Cancer science. 106(7):797-802.
Abstract
Steady-state hematopoiesis responds to extracellular stimuli to meet changing demands and also to pathologically-altered intracellular signaling. Granulocyte production increases upon infection or in response to cytokine stimulation, and activation of the C/EBPβ transcription factor is required for such stress-induced granulopoiesis, whereas C/EBPα plays a critical role in maintaining steady-state granulopoiesis. Such different roles of these C/EBP transcription factors in different modes of hematopoiesis are evolutionally conserved from zebrafish to humans. In addition to reactions against infections, C/EBPβ is responsible for cancer-driven myelopoiesis, which promotes cancer progression at least in part by abrogating the immune response in the cancer microenvironment. The BCR-ABL fusion protein activates emergency-specific pathway of granulopoiesis by up-regulating C/EBPβ. This in turn causes chronic phase chronic myeloid leukemia, which is characterized by myeloid expansion. C/EBPβ also plays a role in other hematological malignancies of both myeloid- and lymphoid lineage-origin. Thus, elucidation of the upstream and downstream networks surrounding C/EBPβ will lead to the development of novel therapeutic strategies for diseases mediated by non-steady-state hematopoiesis. This article is protected by copyright. All rights reserved.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping