ArticleMolecular & cellular proteomics : MCP2014
Suberoylanilide hydroxamic acid (SAHA)-induced dynamics of a human histone deacetylase protein interaction network.
Article in Molecular & cellular proteomics : MCP, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Targeting HDAC and proteostasis to eradicate quiescent cancer cells.Cancer gene therapy · 2026Article
- Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation.Cell death & disease · 2026Article
- A genome-wide CRISPR screen identifies the TNRC18 gene locus as a regulator of inflammatory signaling.Nature communications · 2025Article
- Epigenetic Remodeling in Thyroid Cancer: New Dimensions of Targeted Therapy Through lncRNA Modulation.Current issues in molecular biology · 2025Article
- BAHCC1 binds H4K20me1 to facilitate the MCM complex loading and DNA replication.Nature communications · 2025Article
- Role of the NuRD complex and altered proteostasis in cancer cell quiescence.bioRxiv : the preprint server for biology · 2025Article
- Polycomb Repressive Complex 2 in Oncology.Cancer treatment and research · 2023Article
- Epigenetic Silencing of BMP6 by the SIN3A-HDAC1/2 Repressor Complex Drives Melanoma Metastasis via FAM83G/PAWS1.Molecular cancer research : MCR · 2022Article
- Article
- Generating topological protein interaction scores and data visualization with TopS.Methods (San Diego, Calif.) · 2020Article
- BAHCC1 binds H3K27me3 via a conserved BAH module to mediate gene silencing and oncogenesis.Nature genetics · 2020Article
- Integrative Modeling of a Sin3/HDAC Complex Sub-structure.Cell reports · 2020Article
- Focus-ING on DNA Integrity: Implication of ING Proteins in Cell Cycle Regulation and DNA Repair Modulation.Cancers · 2019Review
- Physical and functional interaction between SET1/COMPASS complex component CFP-1 and a Sin3S HDAC complex in C. elegans.Nucleic acids research · 2019Article
- Exploiting ING2 Epigenetic Modulation as a Therapeutic Opportunity for Non-Small Cell Lung Cancer.Cancers · 2019Review
- A Structured Workflow for Mapping Human Sin3 Histone Deacetylase Complex Interactions Using Halo-MudPIT Affinity-Purification Mass Spectrometry.Molecular & cellular proteomics : MCP · 2018Article
- Unravelling the biology of chromatin in health and cancer using proteomic approaches.Expert review of proteomics · 2017Review
- Fam60a defines a variant Sin3a-Hdac complex in embryonic stem cells required for self-renewal.The EMBO journal · 2017Article
- Identification of Topological Network Modules in Perturbed Protein Interaction Networks.Scientific reports · 2017Article
- There is no human interactome.Genome biology · 2016Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylases (HDACs) are targets for cancer therapy. Suberoylanilide hydroxamic acid (SAHA) is an HDAC inhibitor approved by the U.S. Food and Drug Administration for the treatment of cutaneous T-cell lymphoma. To obtain a better mechanistic understanding of the Sin3/HDAC complex in cancer, we extended its protein-protein interaction network and identified a mutually exclusive pair within the complex. We then assessed the effects of SAHA on the disruption of the complex network through six homologous baits. SAHA perturbs multiple protein interactions and therefore compromises the composition of large parts of the Sin3/HDAC network. A comparison of the effect of SAHA treatment on gene expression in breast cancer cells to a knockdown of the ING2 subunit indicated that a portion of the anticancer effects of SAHA may be attributed to the disruption of ING2's association with the complex. Our dynamic protein interaction network resource provides novel insights into the molecular mechanism of SAHA action and demonstrates the potential for drugs to rewire networks.
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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.