ArticleBreast cancer research : BCR2018
Induction of cell cycle arrest and inflammatory genes by combined treatment with epigenetic, differentiating, and chemotherapeutic agents in triple-negative breast cancer.
Article in Breast cancer research : BCR, 2018. 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, 25 citations in OpenAlex.
- Entinostat plus Pembrolizumab in Patients with Metastatic NSCLC Previously Treated with Anti-PD-(L)1 Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Trial
- The retinol-metabolizing enzyme DHRS3 coordinates antigen presentation, endothelial stability, and cholesterol metabolism to suppress hepatocellular carcinoma progression.The Journal of biological chemistry · 2026Article
- Review
- CRYβB2 is a biomarker for poor prognosis and response to CDK4/6 inhibitors in breast cancer.Breast cancer research : BCR · 2026Article
- Unlocking the epigenetic code: new insights into triple-negative breast cancer.Frontiers in oncology · 2024Review
- Inhibition of histone deacetylases attenuates tumor progression and improves immunotherapy in breast cancer.Frontiers in immunology · 2023Review
- Systems Drug Design for Muscle Invasive Bladder Cancer and Advanced Bladder Cancer by Genome-Wide Microarray Data and Deep Learning Method with Drug Design Specifications.International journal of molecular sciences · 2022Article
- Review
- Histone methyltransferase SETD1A participates in lung cancer progression.Thoracic cancer · 2021Article
- Nutraceuticals in the Mediterranean Diet: Potential Avenues for Breast Cancer Treatment.Nutrients · 2021Review
- Mitosis in Cancer Cell Increases Immune Resistance via High Expression of HLA-G and PD-L1.Cancers · 2020Article
- Epigenetic polypharmacology: A new frontier for epi-drug discovery.Medicinal research reviews · 2020Review
- Understanding the Mechanisms by Which Epigenetic Modifiers Avert Therapy Resistance in Cancer.Frontiers in oncology · 2020Review
- Identification of potential key genes and pathways predicting pathogenesis and prognosis for triple-negative breast cancer.Cancer cell international · 2019Article
- Anti-Proliferative and Pro-Apoptotic Effects ofJournal of evidence-based integrative medicineArticle
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA combination of entinostat, all-trans retinoic acid, and doxorubicin (EAD) induces cell death and differentiation and causes significant regression of xenografts of triple-negative breast cancer (TNBC).
methodsWe investigated the mechanisms underlying the antitumor effects of each component of the EAD combination therapy by high-throughput gene expression profiling of drug-treated cells.
resultsMicroarray analysis showed that entinostat and doxorubicin (ED) altered expression of genes related to growth arrest, inflammation, and differentiation. ED downregulated MYC, E2F, and G2M cell cycle genes. Accordingly, entinostat sensitized the cells to doxorubicin-induced growth arrest at G2. ED induced interferon genes, which correlated with breast tumors containing a higher proportion of tumor-infiltrating lymphocytes. ED also increased the expression of immune checkpoint agonists and cancer testis antigens. Analysis of TNBC xenografts showed that EAD enhanced the inflammation score in nude mice. Among the genes differentially regulated between the EAD and ED groups, an all-trans retinoic acid (ATRA)-regulated gene, DHRS3, was induced in EAD-treated xenografts. DHRS3 was expressed at lower levels in human TNBC metastases compared to normal breast or primary tumors. High expression of ED-induced growth arrest and inflammatory genes was associated with better prognosis in TNBC patients.
conclusionsEntinostat potentiated doxorubicin-mediated cell death and the combination induced inflammatory signatures. The ED-induced immunomodulation may improve immunotherapy. Addition of ATRA to ED may potentiate inflammation and contribute to TNBC regression.
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