ArticleOncology letters2019
Upregulation of FoxP4 in HCC promotes migration and invasion through regulation of EMT.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
38 citing papers in PubMed, 66 citations in OpenAlex.
- Systematic analysis of the mitophagy scoring system in the prognosis and immunotherapy of HCC patients.Discover oncology · 2026Article
- FAIM modulates HCC progression via enhancing HMGA1 interaction with CDK7 and promoting its phosphorylation level.Journal of translational medicine · 2025Article
- Transcription Factor TCF12 Activates the Transcription Level of SLC38A1 to Promote the Development of Hepatocellular Carcinoma.Applied biochemistry and biotechnology · 2025Article
- Cox-Sage: enhancing Cox proportional hazards model with interpretable graph neural networks for cancer prognosis.Briefings in bioinformatics · 2025Article
- Construction and validation of transcription‑factor‑based prognostic signature for TACE non‑response and characterization of tumor microenvironment infiltration in hepatocellular carcinoma.Oncology letters · 2025Article
- Prediction and assessment of deleterious and disease causing nonsynonymous single nucleotide polymorphisms (nsSNPs) in humanHeliyon · 2024Article
- FOXP4-mediated induction of PTK7 activates the Wnt/β-catenin pathway and promotes ovarian cancer development.Cell death & disease · 2024Article
- Elucidating hepatocellular carcinoma progression: a novel prognostic miRNA-mRNA network and signature analysis.Scientific reports · 2024Article
- Comprehensive Analysis of TICRR in Hepatocellular Carcinoma Based on Bioinformatics Analysis.Biochemical genetics · 2024Article
- Transcription factor FOXP4 inversely governs tumor suppressor genes and contributes to thyroid cancer progression.Heliyon · 2024Article
- Incomplete Thermal Ablation-Induced FOXP4-Mediated Promotion of Malignant Progression in Liver Cancer via NDST2.Journal of hepatocellular carcinoma · 2024Article
- METTL14 Induced NJournal of Cancer · 2024Article
- Hsa_circ_0017956 Acts as miR-758-3p Sponge to Facilitate the Progression of Non-small-Cell Lung Cancer by Regulating FOXP4 Expression.Molecular biotechnology · 2023Article
- CircUSP10 promotes liver cancer progression by regulating miR-211-5p/TCF12/EMT signaling pathway.Heliyon · 2023Article
- The essential role of forkhead box P4 (FOXP4) in thyroid cancer: a study related to The Cancer Genome Atlas and experimental data.Endocrine connections · 2023Article
- [Eriocitrin suppresses proliferation and migration of hepatocellular carcinoma SMMC-7721 cells by promoting ROS production and activating the MAPK pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Camptothecin improves sorafenib sensitivity by inhibiting Nrf2‑ARE pathway in hepatocellular carcinoma.Oncology reports · 2023Article
- Article
- Article
- MiR-4521 plays a tumor repressive role in growth and metastasis of hepatocarcinoma cells by suppressing phosphorylation of FAK/AKT pathway via targeting FAM129A.Journal of advanced research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have indicated that FoxP1, FoxP2 and FoxP3 play important roles in hepatocellular carcinoma (HCC). However, the effect of FoxP4 in HCC requires further elucidation. The aim of the present study was to explore the roles of FoxP4 in HCC and further decipher the detailed mechanism. In present study, it was found that FoxP4, which is overexpressed in HCC tissues and cell lines, facilitated EMT in HCC cell lines through regulation of Slug. First, increased expression of FoxP4 was identified in 110 pairs of human HCC tumor and their adjacent normal tissues. In addition, the association between FoxP4 expression and clinicopathological features of HCC patients indicated that FoxP4 played vital roles in HCC development. Subsequently, gain- and loss-of-function experiments indicated that FoxP4 promoted cellular proliferation, migration as well invasion. In addition, EMT, a key mechanism during cancer metastasis, was regulated by FoxP4. Furthermore, ChIP and qChIP as well as luciferase reporter assays indicated that Slug, an EMT-associated transcription factor, was transcriptionally regulated by FoxP4. In conclusion, FoxP4 functioned as a tumor promoter in HCC cells by transcriptionally regulating Slug, and the present study highlighted the potential effects of FoxP4 on the prognosis and treatment of HCC.
Indexed as
Identifiers
What OpenQuestion holds
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.