ArticleBritish journal of cancer2023
HDAC5 modulates SATB1 transcriptional activity to promote lung adenocarcinoma.
Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Histone deacetylases: Function in tumor development and therapeutic prospects (Review).Oncology letters · 2026Review
- HDAC5 stabilization by tubeimoside I suppresses cervical cancer metastasis via inhibiting H3K27ac/KPNA2 axis.British journal of cancer · 2026Article
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Macrophages: emerging targets for ulcerative colitis.Frontiers in immunology · 2025Review
- SATB1 in cancer progression and metastasis: mechanisms and therapeutic potential.Frontiers in oncology · 2025Review
- Association of changes in expression ofEpigenetics · 2024Article
- Temporal regulation of acetylation status determines PARP1 role in DNA damage response and metabolic homeostasis.Science advances · 2024Article
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
backgroundDysregulation of histone deacetylases has been linked to diverse cancers. HDAC5 is a histone deacetylase belonging to Class IIa family of histone deacetylases. Limited substrate repertoire restricts the understanding of molecular mechanisms underlying its role in tumorigenesis.
methodsWe employed a biochemical screen to identify SATB1 as HDAC5-interacting protein. Coimmunoprecipitation and deacetylation assay were performed to validate SATB1 as a HDAC5 substrate. Proliferation, migration assay and xenograft studies were performed to determine the effect of HDAC5-SATB1 interaction on tumorigenesis.
resultsHere we report that HDAC5 binds to and deacetylates SATB1 at the conserved lysine 411 residue. Furthermore, dynamic regulation of acetylation at this site is determined by TIP60 acetyltransferase. We also established that HDAC5-mediated deacetylation is critical for SATB1-dependent downregulation of key tumor suppressor genes. Deacetylated SATB1 also represses SDHA-induced epigenetic remodeling and anti-proliferative transcriptional program. Thus, SATB1 spurs malignant phenotype in a HDAC5-dependent manner.
conclusionsOur study highlights the pivotal role of HDAC5 in tumorigenesis. Our findings provide key insights into molecular mechanisms underlying SATB1 promoted tumor growth and metastasis.
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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.