ArticleOncotarget2015
Induction of USP17 by combining BET and HDAC inhibitors in breast cancer cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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Who cites it
50 citing papers in PubMed, 79 citations in OpenAlex.
- Article
- Combined inhibition of BETs and HDACs as a potential epigenetics-based therapy for malignant rhabdoid tumor.Cell death & disease · 2026Article
- JQ1 Downregulates IL-20RA Expression in Triple Negative Breast Cancer Cells In Vitro and In Vivo.International journal of molecular sciences · 2026Article
- Steroidogenic Acute Regulatory Protein in Breast Cancer: Mechanistic Insights into Pathogenesis and Therapeutics.International journal of molecular sciences · 2026Review
- Super-enhancers in tumors: unraveling recent advances in their role in Oncogenesis and the emergence of targeted therapies.Journal of translational medicine · 2025Review
- Bromodomain inhibition targeting BPTF in the treatment of melanoma and other solid tumors.Clinical & experimental metastasis · 2024Review
- Bromodomain and extraterminal (BET) proteins: biological functions, diseases, and targeted therapy.Signal transduction and targeted therapy · 2023Review
- Effects of bromodomain and extra-terminal inhibitor JQ1 and interleukin-6 on breast cancer cells.Molecular biology reports · 2023Article
- Metabolic Reprogramming by Ribitol Expands the Therapeutic Window of BETi JQ1 against Breast Cancer.Cancers · 2023Article
- Repurposable Drugs for Immunotherapy and Strategies to Find Candidate Drugs.Pharmaceutics · 2023Review
- Inhibition of histone deacetylases attenuates tumor progression and improves immunotherapy in breast cancer.Frontiers in immunology · 2023Review
- Bromodomain Protein BRD4-Mediated Mutant p53 Transcription Promotes TNBC Progression.International journal of molecular sciences · 2022Article
- Super-enhancer-controlled positive feedback loop BRD4/ERα-RET-ERα promotes ERα-positive breast cancer.Nucleic acids research · 2022Article
- The synergistic anticancer effect of the bromodomain inhibitor OTX015 and histone deacetylase 6 inhibitor WT-161 in osteosarcoma.Cancer cell international · 2022Article
- BET Proteins as Attractive Targets for Cancer Therapeutics.International journal of molecular sciences · 2021Review
- The role of the deubiquitinating enzyme DUB3/USP17 in cancer: a narrative review.Cancer cell international · 2021Review
- Bromodomain-containing protein BRPF1 is a therapeutic target for liver cancer.Communications biology · 2021Article
- Chemogenomics for drug discovery: clinical molecules from open access chemical probes.RSC chemical biology · 2021Review
- Targeting Histone Modifications in Breast Cancer: A Precise Weapon on the Way.Frontiers in cell and developmental biology · 2021Review
- ARID1A Mutation in Metastatic Breast Cancer: A Potential Therapeutic Target.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the bromodomain and extra-C terminal (BET) domain protein family and the histone deacetylase (HDAC) enzyme family regulate the expression of important oncogenes and tumor suppressor genes. Here we show that the BET inhibitor JQ1 inhibits proliferation and induces apoptosis of both triple negative and estrogen receptor positive breast cancer cells. Consistent with the critical role of histone acetylation in the regulation of gene expression, treatment with JQ1 or the HDAC inhibitor mocetinostat was associated with global changes in gene expression resulting in suppression of genes involved in cell-cycle regulation. Combining JQ1 with mocetinostat, further decreased cell viability. This synergistic effect was associated with increased suppression of genes essential for cell-cycle progression. Furthermore, we detected dramatic increase in the expression of several members of the ubiquitin-specific protease 17 (USP17) family of deubiquitinating enzymes in response to the combination treatment. Increased expression of USP17 enzymes were able to attenuate the Ras/MAPK pathway causing decrease in cell viability, while, siRNA mediated depletion of USP17 significantly decreased cytotoxicity after the combination treatment. In conclusion, our study demonstrates that co-treatment with BET inhibitors and HDAC inhibitors reduces breast cancer cell viability through induction of USP17.
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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.