ArticleOncogene2017
Foxp3 is a key downstream regulator of p53-mediated cellular senescence.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- USP7 at the Crossroads of Ubiquitin Signaling, Cell Cycle, and Tumorigenesis.Molecules (Basel, Switzerland) · 2025Review
- GDF11 downregulates FOXP3 in T-cell acute lymphoblastic leukemia-derived cells and associates with restraining aggressiveness.Oncology research · 2025Article
- Activating transcription factor 3 mediates apoptosis and cell cycle arrest in TP53-mutated anaplastic thyroid cancer cells.Thyroid research · 2024Article
- Advances in Foxp3+ regulatory T cells (Foxp3+ Treg) and key factors in digestive malignancies.Frontiers in immunology · 2024Review
- Evaluating the effect of LPS from periodontal pathogenic bacteria on the expression of senescence-related genes in human dental pulp stem cells.Journal of cellular and molecular medicine · 2022Article
- Article
- Negative Immune Checkpoint Protein, VISTA, Regulates the CD4Frontiers in immunology · 2022Article
- Forkhead Box Protein P3 (FOXP3) Represses ATF3 Transcriptional Activity.International journal of molecular sciences · 2021Article
- The Common GermlineCancer research · 2021Article
- Nuclear FOXP3 inhibits tumor growth and induced apoptosis in hepatocellular carcinoma by targeting c-Myc.Oncogenesis · 2020Article
- The RNA-Binding Protein HuR in Digestive System Tumors.BioMed research international · 2020Review
- Molecular networks of FOXP family: dual biologic functions, interplay with other molecules and clinical implications in cancer progression.Molecular cancer · 2019Review
- FOXP3 inhibits MYC expression via regulating miR-198 and influences cell viability, proliferation and cell apoptosis in HepG2.Cancer medicine · 2018Article
- Repeated stimulation by LPS promotes the senescence of DPSCs via TLR4/MyD88-NF-κB-p53/p21 signaling.Cytotechnology · 2018Article
- Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?Cellular and molecular life sciences : CMLS · 2017Review
- Modeling cancer driver events in vitro using barrier bypass-clonal expansion assays and massively parallel sequencing.Oncogene · 2017Article
- Redox control of senescence and age-related disease.Redox biology · 2017Review
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The downstream events and target genes of p53 in the process of senescence are not fully understood. Here, we report a novel function of the forkhead transcription factor Foxp3, which is a key player in mediating T-cell inhibitory functions, in p53-mediated cellular senescence. The overexpression of Foxp3 in mouse embryonic fibroblasts (MEFs) accelerates senescence, whereas Foxp3 knockdown leads to escape from p53-mediated senescence in p53-expressing MEFs. Consistent with these results, Foxp3 expression resulted in the induction of senescence in epithelial cancer cells, including MCF7 and HCT116 cells. Foxp3 overexpression also increased the intracellular levels of reactive oxygen species (ROS). The ROS inhibitor N-acetyl-l-cysteine rescued cells from Foxp3-expression-induced senescence. Furthermore, the elevated ROS levels that accompanied Foxp3 overexpression were paralleled by an increase in p21 expression. Knockdown of p21 in Foxp3-expressing MEFs abrogated the Foxp3-dependent increase in ROS levels, indicating that Foxp3 acts through the induction of p21 and the subsequent ROS elevation to trigger senescence. Collectively, these results suggest that Foxp3 is a downstream target of p53 that is sufficient to induce p21 expression, ROS production and p53-mediated senescence.
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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.