ArticleBreast cancer research : BCR2015
HDAC6 activity is a non-oncogene addiction hub for inflammatory breast cancers.
Article in Breast cancer research : BCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 52 citations in OpenAlex.
- Single-cell multi-omic profiling of heterogeneous PROCRiScience · 2026Article
- Single-cell transcriptome analysis reveals the malignant characteristics of tumour cells and the immunosuppressive landscape in HER2-positive inflammatory breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025Review
- Regulation of HDAC6 Catalytic Activity in Cancer: The Role of Post-Translational Modifications and Protein-Protein Interactions.International journal of molecular sciences · 2025Review
- AGBL2 promotes renal cell carcinoma cells proliferation and migration via α-tubulin detyrosination.Heliyon · 2024Article
- Selective inhibition of HDAC6 promotes bladder cancer radiosensitization and mitigates the radiation-induced CXCL1 signalling.British journal of cancer · 2023Article
- Network-based assessment of HDAC6 activity predicts preclinical and clinical responses to the HDAC6 inhibitor ricolinostat in breast cancer.Nature cancer · 2023Article
- HDAC6 score: to treat or not to treat?Nature cancer · 2023Article
- HDAC6: A unique HDAC family member as a cancer target.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Single-cell analysis reveals the Comma-1D cell line as a unique model for mammary gland development and breast cancer.Journal of cell science · 2022Article
- Uveal Melanoma Cell Line Proliferation Is Inhibited by Ricolinostat, a Histone Deacetylase Inhibitor.Cancers · 2022Article
- HDAC6 inhibition reverses long-term doxorubicin-induced cognitive dysfunction by restoring microglia homeostasis and synaptic integrity.Theranostics · 2022Article
- Shifting the paradigm in treating multi-factorial diseases: polypharmacological co-inhibitors of HDAC6.RSC medicinal chemistry · 2021Review
- Network-based systems pharmacology reveals heterogeneity in LCK and BCL2 signaling and therapeutic sensitivity of T-cell acute lymphoblastic leukemia.Nature cancer · 2021Article
- HDAC6-selective inhibitors enhance anticancer effects of paclitaxel in ovarian cancer cells.Oncology letters · 2021Article
- HDAC6 inhibition enhances the anti-tumor effect of eribulin through tubulin acetylation in triple-negative breast cancer cells.Breast cancer research and treatment · 2021Article
- HDAC6/HNF4α loop mediated by miR-1 promotes bile acids-induced gastric intestinal metaplasia.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2021Article
- The Tubulin Code in Mitosis and Cancer.Cells · 2020Review
- Epigenetics in Inflammatory Breast Cancer: Biological Features and Therapeutic Perspectives.Cells · 2020Review
- Review
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 8 institutions in 2 countries.
Funding
Abstract
introductionInflammatory breast cancer (IBC) is the most lethal form of breast cancers with a 5-year survival rate of only 40 %. Despite its lethality, IBC remains poorly understood which has greatly limited its therapeutic management. We thus decided to utilize an integrative functional genomic strategy to identify the Achilles' heel of IBC cells.
methodsWe have pioneered the development of genetic tools as well as experimental and analytical strategies to perform RNAi-based loss-of-function studies at a genome-wide level. Importantly, we and others have demonstrated that these functional screens are able to identify essential functions linked to certain cancer phenotypes. Thus, we decided to use this approach to identify IBC specific sensitivities.
resultsWe identified and validated HDAC6 as a functionally necessary gene to maintain IBC cell viability, while being non-essential for other breast cancer subtypes. Importantly, small molecule inhibitors for HDAC6 already exist and are in clinical trials for other tumor types. We thus demonstrated that Ricolinostat (ACY1215), a leading HDAC6 inhibitor, efficiently controls IBC cell proliferation both in vitro and in vivo. Critically, functional HDAC6 dependency is not associated with genomic alterations at its locus and thus represents a non-oncogene addiction. Despite HDAC6 not being overexpressed, we found that its activity is significantly higher in IBC compared to non-IBC cells, suggesting a possible rationale supporting the observed dependency.
conclusionOur finding that IBC cells are sensitive to HDAC6 inhibition provides a foundation to rapidly develop novel, efficient, and well-tolerated targeted therapy strategies for IBC patients.
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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.