ArticleTranslational cancer research2020
FOXP3 expression in FOXP3
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- FKH domain-mediated nuclear FOXP3 suppresses gastric cancer malignancy via c-MYC/CDKN1A regulation, EMT inhibition, and PI3K/AKT signaling modulation.Molecular and cellular biochemistry · 2026Article
- Mechanism of METTL14 regulates HBV-HCC malignant progression by mediating m6A modification of FOXP3 and thus transcriptional activation of ALDOB.Journal of molecular histology · 2025Article
- Cholesterol and Immune Microenvironment: Path Towards Tumorigenesis.Current nutrition reports · 2024Review
- Targeting FOXP3 Tumor-Intrinsic Effects Using Adenoviral Vectors in Experimental Breast Cancer.Viruses · 2023Article
- The Role of FOXP3 on Tumor Metastasis and Its Interaction with Traditional Chinese Medicine.Molecules (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundForkhead transcription factor 3 (FOXP3) is a key molecule for the development of regulatory T cell. Recent studies showed that FOXP3 was also expressed in tumor cells. This study is designed to identify the expression of FOXP3 and its pathogenesis in hepatocellular carcinoma (HCC).
methodsThrough immunohistochemistry, RNA extraction and Real-Time Quantitative PCR, western blot analysis, transwell cell migration assay and invasion assays, and
resultsThe results showed that FOXP3 was expressed in partial HCC tissues samples and cell lines. The distant metastasis rate was remarkably higher in the FOXP3 positive HCCs than that in the negative group. The positive rate of FOXP3 expression in the metastatic HCC was higher than that in primary HCC, and the expression level of FOXP3 was found to increase as the enhancement in the metastatic potential of the cell lines. Furthermore, in HCC cell lines, FOXP3 overexpression can promote the cell metastasis and invasion by regulating MMP-1. The
conclusionsOur findings support that partial HCC tissues and cell lines expressing FOXP3 can promote the metastasis by regulating MMP-1.
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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.