ArticleCell death & disease2018
C/EBPβ deletion in oncogenic Ras skin tumors is a synthetic lethal event.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- The transcription factor C/EBPβ promotes hyperglycemia-elicited glycolysis and liver cancer progression.Nature communications · 2026Article
- CEBPB-high dormant tumor cells drive immune evasion via S100A8 orchestrated tumor-associated macrophages reprogramming.Theranostics · 2026Article
- Conditional knockout of C/EBPβ in epidermis results in dysregulated lipid biosynthesis and a defect in skin barrier function.PloS one · 2025Article
- 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
- Design and Evaluation of RNA Aptamer-Mediated Delivery of C/EBPJournal of nucleic acids · 2025Article
- CCAAT/Enhancer-Binding Protein β (C/EBPβ) Regulates Calcium Deposition in Smooth Muscle Cells.International journal of molecular sciences · 2024Article
- Scavenger receptor BI attenuates oxidized phospholipid-induced pulmonary inflammation.Toxicology and applied pharmacology · 2023Article
- Review
- Emerging functions of C/EBPβ in breast cancer.Frontiers in oncology · 2023Review
- C/EBPβ deficiency enhances the keratinocyte innate immune response to direct activators of cytosolic pattern recognition receptors.Innate immunity · 2023Article
- Anticancer Activity of ST101, A Novel Antagonist of CCAAT/Enhancer Binding Protein β.Molecular cancer therapeutics · 2022Article
- Targeting IKKε in Androgen-Independent Prostate Cancer Causes Phenotypic Senescence and Genomic Instability.Molecular cancer therapeutics · 2022Article
- C/EBPβ promotes the expression of atrophy-inducing factors by tumours and is a central regulator of cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2022Article
- RAS induced senescence of skin keratinocytes is mediated through Rho-associated protein kinase (ROCK).Molecular carcinogenesis · 2021Article
- Cell-Penetrating CEBPB and CEBPD Leucine Zipper Decoys as Broadly Acting Anti-Cancer Agents.Cancers · 2021Article
- AfterNeuro-oncology advances · 2020Review
- The Mir181ab1 cluster promotes KRAS-driven oncogenesis and progression in lung and pancreas.The Journal of clinical investigation · 2020Article
- The role of noncoding RNAs in epithelial cancer.Cell death discovery · 2020Review
- C/EBPβ suppresses keratinocyte autonomous type 1 IFN response and p53 to increase cell survival and susceptibility to UVB-induced skin cancer.Carcinogenesis · 2019Article
- Multi-omics profiling of calcium-induced human keratinocytes differentiation reveals modulation of unfolded protein response signaling pathways.Cell cycle (Georgetown, Tex.) · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Therapeutic targeting of specific genetic changes in cancer has proven to be an effective therapy and the concept of synthetic lethality has emerged. CCAAT/enhancer-binding protein-β (C/EBPβ), a basic leucine zipper transcription factor, has important roles in cellular processes including differentiation, inflammation, survival, and energy metabolism. Using a genetically engineered mouse model, we report that the deletion C/EBPβ in pre-existing oncogenic Ha-Ras mouse skin tumors in vivo resulted in rapid tumor regression. Regressing tumors exhibited elevated levels of apoptosis and p53 protein/activity, while adjacent C/EBPβ-deleted skin did not. These results indicate that the deletion of C/EBPβ de-represses p53 in oncogenic Ras tumors but not in normal wild-type Ras keratinocytes, and that C/EBPβ is essential for survival of oncogenic Ras tumors. Co-deletion of C/EBPβ and p53 in oncogenic Ras tumors showed p53 is required for tumor regression and elevated apoptosis. In tumors, loss of a pathway that confers adaptability to a stress phenotype of cancer/tumorigenesis, such as DNA damage, could result in selective tumor cell killing. Our results show that oncogenic Ras tumors display a significant DNA damage/replicative stress phenotype and these tumors have acquired a dependence on C/EBPβ for their survival. RNAseq data analysis of regressing tumors deleted of C/EBPβ indicates a novel interface between p53, type-1 interferon response, and death receptor pathways, which function in concert to produce activation of extrinsic apoptosis pathways. In summary, the deletion of C/EBPβ in oncogenic Ras skin tumors is a synthetic lethal event, making it a promising target for future potential anticancer therapies.
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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.