ArticleCommunications biology2023
SERPINA3-ANKRD11-HDAC3 pathway induced aromatase inhibitor resistance in breast cancer can be reversed by HDAC3 inhibition.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Integrated Multi-Omics Reveals Cellular States and Microenvironmental Remodeling in Coexisting DCIS and IDC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- An AI-Assisted Workflow for Rapid Prioritization of FDA-Approved Drugs as HDAC3 Inhibitor Candidates for Drug Repurposing.Biology · 2026Article
- Tamoxifen-pretreated MSC exosomes promote endocrine resistance in ER-positive breast cancer cells through the miR-137/Serpina3 axis: a mechanistic study.Breast cancer research : BCR · 2026Article
- Mechanisms of the Antiproliferative Effects of SIRT6 Inhibition in Melanoma: A Multi-Omics Analysis.Cancers · 2026Article
- AMICI: Attention Mechanism Interpretation of Cell-cell Interactions.bioRxiv : the preprint server for biology · 2025Article
- KBG syndrome-associated protein ANKRD11 regulates SETD5 expression to modulate rRNA levels and translation.iScience · 2025Article
- The role of ankyrin repeat-containing proteins in epigenetic and transcriptional regulation.Cell death discovery · 2025Review
- A short overview of dual targeting HDAC inhibitors.Future medicinal chemistry · 2025Article
- PARD6A promotes lung adenocarcinoma cell proliferation and invasion through Serpina3.Cancer gene therapy · 2024Article
- Molecular features of luminal breast cancer defined through spatial and single-cell transcriptomics.Clinical and translational medicine · 2024Article
- HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endocrine resistance is a major challenge for breast cancer therapy. To identify the genes pivotal for endocrine-resistance progression, we screened five datasets and found 7 commonly dysregulated genes in endocrine-resistant breast cancer cells. Here we show that downregulation of serine protease inhibitor clade A member 3 (SERPINA3) which is a direct target gene of estrogen receptor α contributes to aromatase inhibitor resistance. Ankyrin repeat domain containing 11 (ANKRD11) works as a downstream effector of SERPINA3 in mediating endocrine-resistance. It induces aromatase inhibitor insensitivity by interacting with histone deacetylase 3 (HDAC3) and upregulating its activity. Our study suggests that aromatase inhibitor therapy downregulates SERPINA3 and leads to the ensuing upregulation of ANKRD11, which in turn promotes aromatase inhibitor resistance via binding to and activating HDAC3. HDAC3 inhibition may reverse the aromatase inhibitor resistance in ER-positive breast cancer with decreased SERPINA3 and increased ANKRD11 expression.
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