ArticleAnimal models and experimental medicine2025
FOXK1 promotes hormonally responsive breast carcinogenesis by suppressing apoptosis.
Article in Animal models and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- FOXK1 promotes hormonally responsive breast carcinogenesis by suppressing apoptosis.Animal models and experimental medicine · 2025Article
- Single-cell analysis of tumor microenvironment and cell adhesion reveals that interleukin-1 beta promotes cancer cell proliferation in breast cancer.Animal models and experimental medicine · 2024Article
- FOXK2 targeting by the SCF-E3 ligase subunit FBXO24 for ubiquitin mediated degradation modulates mitochondrial respiration.The Journal of biological chemistry · 2024Article
- Genome-wide DNA methylation profiling of blood samples from patients with major depressive disorder: correlation with symptom heterogeneity.Journal of psychiatry & neuroscience : JPNArticle
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundGlobally, breast cancer constitutes the predominant malignancy in women. Abnormal regulation of epigenetic factors plays a key role in the development of tumors. Anti-apoptosis is a characteristic of tumor cells. Therefore, exploring and identifying relevant epigenetic factors that regulate the apoptosis of tumor cells is the foundation for clarifying the pathogenesis of tumors and achieving precision antitumor therapy.
methodThis study focused on exploring the epigenetic mechanism of FOXK1 in the development of estrogen receptor-positive (ER
resultsFOXK1 interacts with the REST/CoREST transcriptional corepression complex to transcriptionally inhibit target genes representing the apoptotic pathway. Abnormally high expression of FOXK1 prevents the apoptosis of ER
conclusionFOXK1 promotes ER
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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.