ArticleNeurotoxicity research2022
TCF3 Induces DNMT1 Expression to Regulate Wnt Signaling Pathway in Glioma.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- miR-138-5p inhibits WiT-49 cell growth in vitro by downregulating TCF3 expression, and suppresses tumorigenesis in vivo.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Article
- Transcription factor 3 enhances hepatocellular carcinoma metastasis by upregulating matrix metalloproteinase-11.World journal of gastrointestinal oncology · 2025Article
- Decoding Molecular Interactions: Unraveling the Crosstalk between the Wnt Pathway and Key Signaling Networks by miRNA in Colorectal Cancer Progression.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Downregulation of ECRG4 by DNMT1 promotes EC growth via IRF3/IFN-γ/miR-29b/DNMT1/ECRG4 positive feedback loop.iScience · 2025Article
- Human Milk Supports Robust Intestinal Organoid Growth, Differentiation, and Homeostatic Cytokine Production.Gastro hep advances · 2024Article
- Comprehensive analysis of mFrontiers in immunology · 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
5 authors at 3 institutions in 1 country.
Funding
Abstract
The epigenetic alteration is widely understood as the key to cancer initiation. Herein, we intended to clarify the role of transcription factor 3 (TCF3) in the development of glioma and the behind epigenetic mechanism. Through bioinformatics analysis, we identified a TCF3-DNA methyltransferase 1 (DNMT1)-secreted frizzled related protein 1 (SFRP1) axis which was differentially expressed and interacted in gliomas. More specifically, TCF3 activated DNMT1 transcription, and DNMT1 repressed SFRP1 expression. TCF3 and DNMT1 were overexpressed, while SFRP1 was downregulated in glioma. Functionally, TCF3 silencing inhibited cell proliferation and migration, and promoted apoptosis, which were reversed by DNMT1. SFRP1 inhibited the tumor supporting effects of DNMT1 on glioma cells. Moreover, TCF3 downregulation or SFRP1 overexpression inhibited tumorigenesis and enhanced apoptosis of glioma cells, while DNMT1 enhanced tumorigenesis and repressed apoptosis in tumor tissues in vivo. The Wnt pathway was a downstream effector of the TCF3-DNMT1-SFRP1 axis. Collectively, this study determined a novel therapeutic target TCF3 for glioma from the perspective of epigenetic alteration via regulation of SFRP1 expression in a DNMT1-dependent manner.
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.