ArticleOncotarget2012
FOXP3, a novel glioblastoma oncosuppressor, affects proliferation and migration.
Article in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 31 citations in OpenAlex.
- Inhibitory co-receptor Lag3 supports Foxp3Immunity · 2024Article
- Blood signatures for second stage human African trypanosomiasis: a transcriptomic approach.BMC medical genomics · 2020Article
- Ectopic FOXP3 Expression Preserves Primitive Features Of Human Hematopoietic Stem Cells While Impairing Functional T Cell Differentiation.Scientific reports · 2017Article
- Foxp3 Reprograms T Cell Metabolism to Function in Low-Glucose, High-Lactate Environments.Cell metabolism · 2017Article
- Forkhead box P3 regulates ARHGAP15 expression and affects migration of glioma cells through the Rac1 signaling pathway.Cancer science · 2017Article
- Immunotherapy with dendritic cells loaded with glioblastoma stem cells: from preclinical to clinical studies.Cancer immunology, immunotherapy : CII · 2016Review
- Tregs in gliomas - the jury is still out.Neuro-oncology · 2015Article
- FOXP3-miR-146-NF-κB Axis and Therapy for Precancerous Lesions in Prostate.Cancer research · 2015Article
- Endogenous FOXP3 inhibits cell proliferation, migration and invasion in glioma cells.International journal of clinical and experimental medicine · 2015Article
- Higher FOXP3-TSDR demethylation rates in adjacent normal tissues in patients with colon cancer were associated with worse survival.Molecular cancer · 2014Article
- FOXP3 over-expression inhibits melanoma tumorigenesis via effects on proliferation and apoptosis.Oncotarget · 2014Article
- SELDI-TOF analysis of glioblastoma cyst fluid is an approach for assessing cellular protein expression.Neurological research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor FOXP3 plays an essential role in regulatory T cell development and function. In addition, it has recently been identified as a tumor suppressor in different cancers. Here, we report that FOXP3 is expressed in normal brain but strongly down-regulated in glioblastoma (GB) and in corresponding GB stem-like cells growing in culture as neurospheres (GB-NS), as evaluated by real time-PCR and confirmed by immunohistochemistry on an independent set of GB. FOXP3 expression was higher in low-grade gliomas than in GB. Interestingly, we also found that neurosphere generation, a feature present in 58% of the GB that we examined, correlated with lower expression of FOXP3 and shorter patient survival. FOXP3 silencing in one GB-NS expressing measurable levels of the gene caused a significant increase in proliferation and migration as well as highly aggressive growth in xenografts. Conversely, FOXP3 over-expression impaired GB-NS migration and proliferation in vitro. We also demonstrated using ChiP that FOXP3 is a transcriptional regulator of p21 and c-MYC supporting the idea that dysregulated expression of these factors is a major mechanism of tumorigenesis driven by the loss of FOXP3 expression in gliomas. These findings support the assertion that FOXP3 exhibits tumor suppressor activity in glioblastomas.
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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.