ArticleMolecular and cellular biology2004
Critical prosurvival roles for C/EBP beta and insulin-like growth factor I in macrophage tumor cells.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- C/EBPβ as a master regulator of inflammasome signaling in neurodegenerative diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Pooled it
- C/EBPβ Deficiency Enhances Keratinocyte Apoptosis after UVB-Induced DNA Damage via Regulation of the Type I IFN and TNF Responses.Frontiers in cell death · 2025Article
- Magnetic Hydroxyapatite Composite Nanoparticles for Augmented Differentiation of MC3T3-E1 Cells for Bone Tissue Engineering.Marine drugs · 2023Article
- C/EBPβ deficiency enhances the keratinocyte innate immune response to direct activators of cytosolic pattern recognition receptors.Innate immunity · 2023Article
- Distinct characteristics of microglia from neurogenic and non-neurogenic regions of the human brain in patients with Mesial Temporal Lobe Epilepsy.Frontiers in cellular neuroscience · 2022Article
- Myeloid transformation byLife science alliance · 2021Article
- Dominant-Negative ATF5 Compromises Cancer Cell Survival by Targeting CEBPB and CEBPD.Molecular cancer research : MCR · 2020Article
- C/EBPβ suppresses keratinocyte autonomous type 1 IFN response and p53 to increase cell survival and susceptibility to UVB-induced skin cancer.Carcinogenesis · 2019Article
- A Protective Role of Aryl Hydrocarbon Receptor Repressor in Inflammation and Tumor Growth.Cancers · 2019Article
- C/EBPβ deletion in oncogenic Ras skin tumors is a synthetic lethal event.Cell death & disease · 2018Article
- CCAAT-enhancer binding protein (C/EBP) β regulates insulin-like growth factor (IGF) 1 expression in porcine liver during prenatal and postnatal development.Molecular and cellular biochemistry · 2015Article
- miR-191 promotes tumorigenesis of human colorectal cancer through targeting C/EBPβ.Oncotarget · 2015Article
- M-CSF increases proliferation and phagocytosis while modulating receptor and transcription factor expression in adult human microglia.Journal of neuroinflammation · 2013Article
- Cidea is an essential transcriptional coactivator regulating mammary gland secretion of milk lipids.Nature medicine · 2012Article
- LIP expression is regulated by IGF-1R signaling and participates in suppression of anoikis.Molecular cancer · 2011Article
- CCAAT/Enhancer-binding protein beta DNA binding is auto-inhibited by multiple elements that also mediate association with p300/CREB-binding protein (CBP).The Journal of biological chemistry · 2010Article
- C/EBP-beta regulates endoplasmic reticulum stress-triggered cell death in mouse and human models.PloS one · 2010Article
- Rapamycin and the transcription factor C/EBPbeta as a switch in osteoclast differentiation: implications for lytic bone diseases.Journal of molecular medicine (Berlin, Germany) · 2010Review
- C/EBPbeta regulates body composition, energy balance-related hormones and tumor growth.Carcinogenesis · 2009Article
- CCAAT/enhancer-binding protein beta: its role in breast cancer and associations with receptor tyrosine kinases.Expert reviews in molecular medicine · 2009Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
One of the hallmarks of leukemic cells is their ability to proliferate and survive in the absence of exogenous growth factors (GFs). However, the molecular mechanisms used by myeloid tumor cells to escape apoptosis are not fully understood. Here we report that Myc/Raf-transformed macrophages require the transcription factor C/EBP beta to prevent cell death. In contrast to wild-type cells, C/EBP beta(-/-) macrophages were completely dependent on macrophage colony-stimulating factor or granulocyte-macrophage colony-stimulating factor for survival and displayed impaired tumorigenicity in vivo. Microarray analysis revealed that C/EBP beta-deficient cells expressed significantly reduced levels of the prosurvival factor insulin-like growth factor I (IGF-I). Overexpression of C/EBP beta stimulated transcription from the IGF-I promoter, indicating that IGF-I is a direct transcriptional target of C/EBP beta. Serological neutralization of IGF-I in C/EBP beta(+/+) tumor cell cultures induced apoptosis, showing that IGF-I functions as an autocrine survival factor in these cells. Macrophage tumor cells derived from IGF-I(-/-) mice were GF dependent, similar to C/EBP beta-deficient cells. Forced expression of either C/EBP beta or IGF-I in C/EBP beta(-/-) bone marrow cells restored Myc/Raf-induced transformation and permitted neoplastic growth without exogenous GFs. Thus, our findings demonstrate that C/EBP beta is essential for oncogenic transformation of macrophages and functions at least in part by regulating expression of the survival factor IGF-I.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.