ArticleNeoplasia (New York, N.Y.)2014
KAT6A, a chromatin modifier from the 8p11-p12 amplicon is a candidate oncogene in luminal breast cancer.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 63 citations in OpenAlex.
- Targeting the Chromatin-Modifying Enzyme, KDM5C, Enhances AKT Inhibition Response in ER+ Breast Cancer.Molecular cancer therapeutics · 2026Article
- Spatial transcriptome revealed associated biomarkers for endocrine therapy response in HR-positive/HER2-negative early breast cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2026Article
- Hierarchical small molecule inhibition of MYST acetyltransferases.Nature communications · 2026Article
- Beyond CDK4/6 Inhibition: Current Strategies in Hormone Receptor-Positive Metastatic Breast Cancer.Current treatment options in oncology · 2026Review
- Biological Activity and Structural Biology of Current KAT6A Inhibitor Chemotypes.Journal of medicinal chemistry · 2026Article
- Histone acetyltransferase KAT6A contributes to colon cancer malignant progression by inhibiting ferroptosis.BMC cancer · 2025Article
- Exploring KAT6 as a therapeutic target in breast cancer: epigenetic approaches for precision medicine.NPJ breast cancer · 2025Review
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- ING5: multifaceted roles beyond tumor suppression in cellular physiology and disease.Epigenetics & chromatin · 2025Review
- Correlation between KAT6A and PD-L1 expression and role of KAT6A in colorectal cancer.World journal of gastrointestinal oncology · 2025Article
- Combined inhibition of KAT6A/B and Menin reverses estrogen receptor-driven gene expression programs in breast cancer.Cell reports. Medicine · 2025Article
- Hierarchical small molecule inhibition of MYST acetyltransferases.bioRxiv : the preprint server for biology · 2025Article
- Histone acetylation modulators in breast cancer.Breast cancer research : BCR · 2025Review
- The Recruitment and Immune Suppression Mechanisms of Myeloid-Derived Suppressor Cells and Their Impact on Bone Metastatic Cancer.Cancer reports (Hoboken, N.J.) · 2025Review
- Emerging opportunities to treat drug-resistant breast cancer: Discovery of novel small-molecule inhibitors against different targets.Frontiers in pharmacology · 2025Review
- KAT6A Condensates Impair PARP1 Trapping of PARP Inhibitors in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Inhibition of lysine acetyltransferase KAT6 in ERNature medicine · 2024Article
- A MOZ-TIF2 leukemia mouse model displays KAT6-dependent H3K23 propionylation and overexpression of a set of active developmental genes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Pharmacological targeting of the cancer epigenome.Nature cancer · 2024Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chromosome 8p11-p12 amplicon is present in 12% to 15% of breast cancers, resulting in an increase in copy number and expression of several chromatin modifiers in these tumors, including KAT6A. Previous analyses in SUM-52 breast cancer cells showed amplification and overexpression of KAT6A, and subsequent RNAi screening identified KAT6A as a potential driving oncogene. KAT6A is a histone acetyltransferase previously identified as a fusion partner with CREB binding protein in acute myeloid leukemia. Knockdown of KAT6A in SUM-52 cells, a luminal breast cancer cell line harboring the amplicon, resulted in reduced growth rate compared to non-silencing controls and profound loss of clonogenic capacity both in mono-layer and in soft agar. The normal cell line MCF10A, however, did not exhibit slower growth with knockdown of KAT6A. SUM-52 cells with KAT6A knockdown formed fewer mammospheres in culture compared to controls, suggesting a possible role for KAT6A in self-renewal. Previous data from our laboratory identified FGFR2 as a driving oncogene in SUM-52 cells. The colony forming efficiency of SUM-52 KAT6A knockdown cells in the presence of FGFR inhibition was significantly reduced compared to cells with KAT6A knockdown only. These data suggest that KAT6A may be a novel oncogene in breast cancers bearing the 8p11-p12 amplicon. While there are other putative oncogenes in the amplicon, the identification of KAT6A as a driving oncogene suggests that chromatin-modifying enzymes are a key class of oncogenes in these cancers, and play an important role in the selection of this amplicon in luminal B breast cancers.
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