ArticleCell death & disease2019
GATA3 recruits UTX for gene transcriptional activation to suppress metastasis of breast cancer.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Epigenetics and One-Carbon Metabolism in Cancer: Mechanisms and Therapeutic Implications.Advances in experimental medicine and biology · 2026Review
- NSUN2 Promotes Cancer Immune Evasion via Its Moonlighting Function Acting on Metabolic Reprogramming.Cancer communications (London, England) · 2026Article
- Histone lysine demethylases in breast cancer: molecular mechanisms, biological functions, and therapeutic intervention.Molecular cancer · 2025Review
- Review
- Transcriptional co-regulator OCA-B/Pou2af1 restricts Th2 differentiation.Frontiers in immunology · 2025Article
- The PRC2 complex epigenetically silences GATA4 to suppress cellular senescence and promote the progression of breast cancer.Translational oncology · 2024Article
- H3K4me1 facilitates promoter-enhancer interactions and gene activation during embryonic stem cell differentiation.Molecular cell · 2024Article
- DNA methylation profiling deciphers three EMT subtypes with distinct prognoses and therapeutic vulnerabilities in breast cancer.Journal of Cancer · 2024Article
- KDM7A-DT induces genotoxic stress, tumorigenesis, and progression of p53 missense mutation-associated invasive breast cancer.Frontiers in oncology · 2024Article
- Article
- Upregulated GATA3/miR205-5p Axis Inhibits MFNG Transcription and Reduces the Malignancy of Triple-Negative Breast Cancer.Cancers · 2022Article
- GATA3 and MDM2 are synthetic lethal in estrogen receptor-positive breast cancers.Communications biology · 2022Article
- HDAC8 suppresses the epithelial phenotype and promotes EMT in chemotherapy-treated basal-like breast cancer.Clinical epigenetics · 2022Article
- GATA3 Exerts Distinct Transcriptional Functions to Regulate Radiation Resistance in A549 and H1299 Cells.Oxidative medicine and cellular longevity · 2022Article
- Review
- Liquid Biopsy as a Diagnostic and Prognostic Tool for Women and Female Dogs with Breast Cancer.Cancers · 2021Article
- The roles of epigenetics in cancer progression and metastasis.The Biochemical journal · 2021Review
- A transcription factor that promotes proliferation, migration, invasion, and epithelial-mesenchymal transition of ovarian cancer cells and its possible mechanisms.Biomedical engineering online · 2021Article
- Review
- Targeting Histone Modifications in Breast Cancer: A Precise Weapon on the Way.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
GATA3 has emerged as a prominent transcription factor required for maintaining mammary-gland homeostasis. GATA3 loss is associated with aggressive breast cancer development, but the mechanism by which breast cancer is affected by the loss of GATA3 function remains unclear. Here, we report that GATA3 expression is positively correlated with the expression of UTX, a histone H3K27 demethylase contained in the MLL4 methyltransferase complex, and that GATA3 recruits the chromatin-remodeling MLL4 complex and interacts directly with UTX, ASH2L, and RBBP5. Using RNA sequencing and chromatin immunoprecipitation and sequencing, we demonstrate that the GATA3/UTX complex synergistically regulates a cohort of genes including Dicer and UTX, which are critically involved in the epithelial-to-mesenchymal transition (EMT). Our results further show that the GATA3-UTX-Dicer axis inhibits EMT, invasion, and metastasis of breast cancer cells in vitro and the dissemination of breast cancer in vivo. Our study implicates the GATA3-UTX-Dicer axis in breast cancer metastasis and provides new mechanistic insights into the pathophysiological function of GATA3.
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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.