ArticleScientific reports2024
TCF7L1 regulates colorectal cancer cell migration by repressing GAS1 expression.
Article in Scientific reports, 2024. 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
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Who cites it
6 citing papers in PubMed.
- Sexually Dimorphic RNA Helicase DDX3Y, But Not DDX3X, Plays a Potential Tumor-Suppressive Role in Colorectal Carcinogenesis in Males.Biochemical genetics · 2026Article
- Integrative analysis and experiments to explore GAS1 as a prognostic target for ovarian cancer based on angiogenesis-related genes.Journal of ovarian research · 2025Article
- Gas1 regulates embryonic tongue muscle proliferation, differentiation and maturation via alternative pathways to Hedgehog signaling.Development (Cambridge, England) · 2025Article
- Multifaceted Cooperation Between WNT and PI3K Signaling Axis through the Long Noncoding RNA SNHG16 and TCF7 in de novo Acute Lymphoblastic Leukemia Patients.Iranian biomedical journal · 2025Article
- Oncogenic KRAS Mutations Confer a Unique Mechanotransduction Response to Peristalsis in Colorectal Cancer Cells.Molecular cancer research : MCR · 2025Article
- A Haplotype GWAS in Syndromic Familial Colorectal Cancer.International journal of molecular sciences · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
Dysregulated Wnt/β-catenin signaling is a common feature of colorectal cancer (CRC). The T-cell factor/lymphoid enhancer factor (TCF/LEF; hereafter, TCF) family of transcription factors are critical regulators of Wnt/β-catenin target gene expression. Of the four TCF family members, TCF7L1 predominantly functions as a transcriptional repressor. Although TCF7L1 has been ascribed an oncogenic role in CRC, only a few target genes whose expression it regulates have been characterized in this cancer. Through transcriptome analyses of TCF7L1 regulated genes, we noted enrichment for those associated with cellular migration. By silencing and overexpressing TCF7L1 in CRC cell lines, we demonstrated that TCF7L1 promoted migration, invasion, and adhesion. We localized TCF7L1 binding across the CRC genome and overlapped enriched regions with transcriptome data to identify candidate target genes. The growth arrest-specific 1 (GAS1) gene was among these and we demonstrated that GAS1 is a critical mediator of TCF7L1-dependent CRC cell migratory phenotypes. Together, these findings uncover a novel role for TCF7L1 in repressing GAS1 expression to enhance migration and invasion of CRC cells.
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Registered trials
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