ArticleInternational journal of cancer2018
Aberrant expression of SETD1A promotes survival and migration of estrogen receptor α-positive breast cancer cells.
Article in International journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- High-throughput proteomics of breast cancer interstitial fluid: identification of tumor subtype-specific serologically relevant biomarkers.Molecular oncology · 2021Trial
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- FOXA2 as a SETD1A-Regulated Driver of Tamoxifen Resistance in Breast Cancer.Oncology research · 2026Article
- Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.Breast cancer research : BCR · 2025Article
- Epigenetic Modulation and Bone Metastasis: Evolving Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Decoding the Epigenome of Breast Cancer.International journal of molecular sciences · 2025Review
- Crosstalk of methylation and tamoxifen in breast cancer (Review).Molecular medicine reports · 2024Review
- Reversal of the tamoxifen‑resistant breast cancer malignant phenotype by proliferation inhibition with bromosulfonamidine amino‑podophyllotoxin.Oncology letters · 2024Article
- The COMPASS complex maintains the metastatic capacity imparted by a subpopulation of cells in UPS.iScience · 2024Article
- Exploring the Spatial Landscape of the Estrogen Receptor Proximal Proteome With Antibody-Based Proximity Labeling.Molecular & cellular proteomics : MCP · 2024Article
- Anlotinib suppresses the DNA damage response by disrupting SETD1A and inducing p53-dependent apoptosis in Transformed Follicular Lymphoma.International journal of medical sciences · 2024Article
- SETD1A-mediated Methylation of H3K4me3 Inhibits Ferroptosis in Non-small Cell Lung Cancer by Regulating the WTAPP1/WTAP Axis.Current medicinal chemistry · 2024Article
- Identification of a novel target of SETD1A histone methyltransferase and the clinical significance in pancreatic cancer.Cancer science · 2023Article
- Epigenetic regulation of Neuregulin 1 promotes breast cancer progression associated to hyperglycemia.Nature communications · 2023Article
- Emerging roles of interactions between ncRNAs and other epigenetic modifications in breast cancer.Frontiers in oncology · 2023Review
- Epigenetic Factors as Etiological Agents, Diagnostic Markers, and Therapeutic Targets for Luminal Breast Cancer.Biomedicines · 2022Review
- Histone modification and histone modification-targeted anti-cancer drugs in breast cancer: Fundamentals and beyond.Frontiers in pharmacology · 2022Review
- SETD1A-SOX2 axis is involved in tamoxifen resistance in estrogen receptor α-positive breast cancer cells.Theranostics · 2022Article
- SETD1A promotes the proliferation and glycolysis of nasopharyngeal carcinoma cells by activating the PI3K/Akt pathway.Open medicine (Warsaw, Poland) · 2022Article
- MicroRNA-1915-3p inhibits cell migration and invasion by targeting SET in non-small-cell lung cancer.BMC cancer · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The histone H3 lysine 4-specific methyltransferase SETD1A is associated with transcription activation and is considered a key epigenetic regulator that modulates the cell cycle and metastasis in triple-negative breast cancer cells. However, the clinical role of SETD1A in estrogen receptor (ER)-positive breast cancer cells remains unclear. Here, we examined whether SETD1A is a potential target for ERα-positive breast cancer therapy. SETD1A expression was upregulated in breast tumor tissue compared to that in normal breast tissue. Moreover, ER-target genes regulated by SETD1A were particularly enriched in cell cycle and cancer pathways. SETD1A is involved in histone H3K4 methylation, subsequent recruitment of ERα, and the establishment of accessible chromatin structure at the enhancer region of ERα target genes. In addition to ERα target genes, other cell survival genes were also downregulated by SETD1A depletion in MCF-7 cells, leading to significant decrease in cell proliferation and migration, and spontaneous induction of apoptosis. We also found that miR-1915-3p functioned as a novel regulator of SETD1A expression in breast cells. Importantly, the growth of tamoxifen-resistant MCF-7 cells was effectively repressed by SETD1A knockdown. These results indicate that SETD1A may serve as a molecular target and prognostic indicator in ERα-positive breast cancer.
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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.