ArticleNature communications2018
C/EBPβ enhances platinum resistance of ovarian cancer cells by reprogramming H3K79 methylation.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 130 citations in OpenAlex.
- Targeting the C/EBPβ-PRAME-EZH2 complex modulates the Netrin-4/AKT axis to inhibit renal cancer tumorigenesis and metastasis.Cell death and differentiation · 2026Article
- Targeting DOT1L Reactivates HERV-K to Drive Cell-Autonomous and Paracrine Senescence in Adenocarcinoma of the Esophagogastric Junction.Cancer research · 2026Article
- Targeted delivery of TGF-β inhibitor via LHRH-NanoTi reverses the NAT10/ac4C-mediated cisplatin-induced immunosuppressive tumor microenvironment in ovarian cancer.Journal of nanobiotechnology · 2026Article
- Platinum-resistant ovarian cancer: From mechanisms to treatment strategies.Genes & diseases · 2026Review
- Targeting epigenetic networks to overcome cisplatin resistance in ovarian cancer: from mechanisms to clinical translation.Journal of ovarian research · 2026Review
- Inflammatory milieu and role of epigenetic modifications in high-grade serous ovarian cancer.Clinical epigenetics · 2026Review
- Ubiquitination degradation of GATA4 by CUL4B promotes ovarian cancer metastasis by inducing lysosomal acidification.Genome biology · 2026Article
- CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer.Cancer communications (London, England) · 2026Article
- Multi-omics Approaches to CCAAT/Enhancer-Binding Protein Beta in Oral Squamous Cell Carcinoma: Crosstalk Between Tumor Cells and Tumor-Associated Macrophages Driving Disease Progression.Current cancer drug targets · 2026Article
- DOT1L inhibition exerts the anti-tumor effect by activating interferon signaling in breast cancer cells.Clinical epigenetics · 2025Article
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- SLC25A10 promotes cisplatin resistance by inhibiting ferroptosis in cervical cancer.Cell death discovery · 2025Article
- CEBPB regulates ERK1/2 activity through SOS1 and contributes to ovarian cancer progression.Medical oncology (Northwood, London, England) · 2025Article
- DNA Methylation in Ph-Negative Myeloproliferative Neoplasms: Prognostic Role and Therapeutic Implications.Current issues in molecular biology · 2025Review
- DOT1L Mediates Stem Cell Maintenance and Represents a Therapeutic Vulnerability in Cancer.Cancer research · 2025Review
- Targeting mitochondria: a novel approach for treating platinum-resistant ovarian cancer.Journal of translational medicine · 2024Review
- DOT1L-mediated RAP80 methylation promotes BRCA1 recruitment to elicit DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- MiR-223-3p in Cancer Development and Cancer Drug Resistance: Same Coin, Different Faces.International journal of molecular sciences · 2024Review
- PARP1-DOT1L transcription axis drives acquired resistance to PARP inhibitor in ovarian cancer.Molecular cancer · 2024Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemoresistance is a major unmet clinical obstacle in ovarian cancer treatment. Epigenetics plays a pivotal role in regulating the malignant phenotype, and has the potential in developing therapeutically valuable targets that improve the dismal outcome of this disease. Here we show that a series of transcription factors, including C/EBPβ, GCM1, and GATA1, could act as potential modulators of histone methylation in tumor cells. Of note, C/EBPβ, an independent prognostic factor for patients with ovarian cancer, mediates an important mechanism through which epigenetic enzyme modifies groups of functionally related genes in a context-dependent manner. By recruiting the methyltransferase DOT1L, C/EBPβ can maintain an open chromatin state by H3K79 methylation of multiple drug-resistance genes, thereby augmenting the chemoresistance of tumor cells. Therefore, we propose a new path against cancer epigenetics in which identifying and targeting the key regulators of epigenetics such as C/EBPβ may provide more precise therapeutic options in ovarian cancer.
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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.