ArticleBritish journal of cancer2019
HDAC5-mediated deacetylation and nuclear localisation of SOX9 is critical for tamoxifen resistance in breast cancer.
Article in British journal of cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Nuclear SOX9 Expression and Short-Term Survival Outcomes in Early-Stage Luminal Breast Cancer: An Immunohistochemical and Retrospective Cohort Analysis.International journal of molecular sciences · 2026Article
- Acetylation in ovarian cancer: mechanistic insights into drug resistance and emerging therapeutic opportunities.Journal of ovarian research · 2026Review
- Article
- HDAC5 stabilization by tubeimoside I suppresses cervical cancer metastasis via inhibiting H3K27ac/KPNA2 axis.British journal of cancer · 2026Article
- Targeting the NAT10-HDAC4 positive feedback loop counteracts immunosuppression in breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- CK2-mediated HDAC5 shuttling regulates DNA end resection through Ku70 deacetylation.Theranostics · 2026Article
- Protein arginine methyltransferase 7-mediated arginine mono-methylation stabilizes SRY-box transcription factor 9 to promote non-small cell lung cancer progression.Molecular biomedicine · 2025Article
- SOX9: an important factor in regulating breast cancer.European journal of medical research · 2025Review
- Functional analysis of the effects of propofol on tamoxifen‑resistant breast cancer cells: Insights into transcriptional regulation.Oncology letters · 2025Article
- Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025Review
- Review
- SOX9: a novel janus-faced regulator in immunity and its promise as a therapeutic target.Frontiers in molecular biosciences · 2025Review
- NUPR1 contributes to endocrine therapy resistance by modulating BIRC5 expression and inducing luminal B-ERBB2Journal of Cancer · 2025Article
- Association of changes in expression ofEpigenetics · 2024Article
- SOX on tumors, a comfort or a constraint?Cell death discovery · 2024Review
- HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- HDAC5 modulates SATB1 transcriptional activity to promote lung adenocarcinoma.British journal of cancer · 2023Article
- Emerging Role of Epigenetic Modifiers in Breast Cancer Pathogenesis and Therapeutic Response.Cancers · 2023Review
- New insights into KLFs and SOXs in cancer pathogenesis, stemness, and therapy.Seminars in cancer biology · 2023Review
- Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTamoxifen resistance remains a significant clinical challenge for the therapy of ER-positive breast cancer. It has been reported that the upregulation of transcription factor SOX9 in ER
methodsThe acetylation level of SOX9 was detected by immunoprecipitation and western blotting. The expressions of HDACs and SIRTs were evaluated by qRT-PCR. Cell growth was measured by performing MTT assay. ALDH-positive breast cancer stem cells were evaluated by flow cytometry. Interaction between HDAC5 and SOX9 was determined by immunoprecipitation assay.
resultsDeacetylation is required for SOX9 nuclear translocation in tamoxifen-resistant breast cancer cells. Furthermore, HDAC5 is the key deacetylase responsible for SOX9 deacetylation and subsequent nuclear translocation. In addition, the transcription factor C-MYC directly promotes the expression of HDAC5 in tamoxifen resistant breast cancer cells. For clinical relevance, high SOX9 and HDAC5 expression are associated with lower survival rates in breast cancer patients treated with tamoxifen.
conclusionsThis study reveals that HDAC5 regulated by C-MYC is essential for SOX9 deacetylation and nuclear localisation, which is critical for tamoxifen resistance. These results indicate a potential therapy strategy for ER
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