ArticleOncotarget2017
C/EBP-δ positively regulates MDSC expansion and endothelial VEGFR2 expression in tumor development.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 16 citations in OpenAlex.
- Basic biology and roles of CEBPD in cardiovascular disease.Cell death discovery · 2025Review
- Myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment and their targeting in cancer therapy.Molecular cancer · 2025Review
- Hypoxia Abrogates Tumor-Suppressive Activities of C/EBPδ in Pancreatic Cancer.International journal of molecular sciences · 2024Article
- Myeloid-derived suppressor cells in cancer.iLIVER · 2022Review
- Tissue-Resident Innate Immune Cell-Based Therapy: A Cornerstone of Immunotherapy Strategies for Cancer Treatment.Frontiers in cell and developmental biology · 2022Review
- Exercise-induced angiogenesis is dependent on metabolically primed ATF3/4Cell metabolism · 2021Article
- [CCAAT/enhancer binding protein δ inhibits invasion and metastasis of liver cancer by regulating M1 type macrophages polarization].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021Article
- Myeloid-Derived Suppressor Cells: A Multifaceted Accomplice in Tumor Progression.Frontiers in cell and developmental biology · 2021Review
- Myeloid-Derived Suppressor Cell Differentiation in Cancer: Transcriptional Regulators and Enhanceosome-Mediated Mechanisms.Frontiers in immunology · 2020Review
- Review
- Identification and Characterization of a Novel Protein ASP-3 Purified fromMarine drugs · 2019Article
- C/EBPδ links IL-6 and HIF-1 signaling to promote breast cancer stem cell-associated phenotypes.Oncogene · 2019Article
- The CCAAT/Enhancer-Binding Protein Family: Its Roles in MDSC Expansion and Function.Frontiers in immunology · 2019Review
- Myeloid-Derived Suppressor Cells and Pulmonary Hypertension.International journal of molecular sciences · 2018Review
- Dual negative roles of C/EBPα in the expansion and pro-tumor functions of MDSCs.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial cells and Gr-1+CD11b+ myeloid derived suppressor cells (MDSCs) are two important components that constitute the tumor microenvironment. Targeting these cells offers the potential to halt tumor growth. In this study, we report a common mediator in C/EBP-δ that regulates both components and aids in tumor development. C/EBP-δ is elevated in tumor derived MDSCs. Interestingly, genetic deletion of C/EBP-δ in mice significantly impaired MDSC expansion in response to tumor progression, but it had no effect on Gr-1+CD11b+ cell production in normal development. It suggests a specific role of C/EBP-δ in emergency myelopoiesis under tumor conditions. Consistent with the pro tumor functions of MDSCs, loss of C/EBP-δ resulted in reduced tumor angiogenesis and tumor growth. Moreover, we found expression of C/EBP-δ in vascular endothelial cells. C/EBP-δ regulated cell motility, endothelial network formation and vascular sprouting. Notably, inactivation of C/EBP-δ in endothelial cells specifically inhibited the expression of VEGFR2 but not VEGFR1. Ectopic expression of C/EBP-δ increased and knockdown of the gene decreased VEGFR2 expression. C/EBP-δ is recruited to the promoter region of VEGFR2, indicative of transcriptional regulation. Collectively, this study has identified a positive mediator in C/EBP-δ, which regulates tumor induced MDSC expansion and VEGFR2 expression in endothelium. Considering the importance of MDSCs and endothelial cells in tumor progression, targeting C/EBP-δ may provide an interesting means for cancer therapy, killing two birds with one stone.
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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.