ArticleInternational journal of clinical and experimental pathology2019
FAT1 inhibits the proliferation and metastasis of cervical cancer cells by binding β-catenin.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- C-MYC as a key effector of WNT, PI3K/AKT, MAPK, and TGF-β signaling pathways in regulation of epithelial-mesenchymal transition during tumor metastasis.Cancer cell international · 2026Review
- Burden of rare genetic variants in genes associated with cancer among Malawian cervical cancer patients.African journal of laboratory medicine · 2026Article
- Loss of FAT1 drives cyclophosphamide resistance in breast cancer via the Wnt/β-Catenin pathway.International journal of biological sciences · 2026Article
- Recent advances in the role of atypical cadherin FAT1 in tumorigenesis (Review).Oncology letters · 2025Review
- Distinct genomic features and mutational signatures of nucleotide excision repair and mismatch repair in thymoma.American journal of cancer research · 2025Article
- FAT1 inhibits the proliferation of DLBCL cells via increasing the mScientific reports · 2024Article
- Article
- α-catenin interaction with YAP/FoxM1/TEAD-induced CEP55 supports liver cancer cell migration.Cell communication and signaling : CCS · 2023Article
- Nivolumab plus chemoradiotherapy in locally-advanced cervical cancer: the NICOL phase 1 trial.Nature communications · 2023Article
- FAT1 expression in T-cell acute lymphoblastic leukemia (T-ALL) modulates proliferation and WNT signaling.Scientific reports · 2023Article
- Epigenetic Alterations of Repeated Relapses in Patient-matched Childhood Ependymomas.Nature communications · 2022Article
- Establishment and genetically characterization of patient-derived xenograft models of cervical cancer.BMC medical genomics · 2022Article
- Analysis of Genetic Alterations in Ocular Adnexal Mucosa-Associated Lymphoid Tissue Lymphoma With Whole-Exome Sequencing.Frontiers in oncology · 2022Article
- Detailed characterization of the transcriptome of single B cells in mantle cell lymphoma suggesting a potential use for SOX4.Scientific reports · 2021Observational
- Role of FAT1 in health and disease.Oncology letters · 2021Review
- Antiproliferative and apoptogenic effects of Cassia fistula L. n-hexane fraction against human cervical cancer (HeLa) cells.Environmental science and pollution research international · 2020Article
- miR-532-3p Inhibits Proliferation and Promotes Apoptosis of Lymphoma Cells by Targeting β-Catenin.Journal of Cancer · 2020Article
- A proteomic atlas of glypican-3 interacting partners: Identification of alpha-fetoprotein and other extracellular proteins as potential immunotherapy targets in liver cancer.Proteoglycan researchArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FAT1 is a mutant gene found frequently in human cervical cancer (CC), but its expression and relevance in CC proliferation, invasion, and migration are still unknown. We aimed to explore the role and novel mechanism of FAT1 in CC progression. The expression of FAT1 in CC and adjacent normal tissues was analysed, and we investigated the proliferation, migration, and invasion of HeLa and C33A cells treated with wild-type FAT1 plasmid or FAT1 siRNA. Meanwhile, we evaluated the effect of FAT1 on the epithelial-mesenchymal transition (EMT) and the β-catenin-mediated transcription of target genes. Here, we showed that FAT1 expression was significantly lower in CC tissues than in adjacent tissues. FAT1 overexpression significantly dysregulated CC cell proliferation, invasion, and migration, whereas FAT1 knockdown had the opposite effect. FAT1 overexpression promoted the expression of phosphorylated β-catenin and E-cadherin protein and inhibited the expression of vimentin, TWIST, and several downstream targets of β-catenin, namely, c-MYC, TCF-4 and MMP14. In contrast, FAT1 silencing notably increased the expression c-MYC, TCF-4, and MMP14 and promoted the EMT in HeLa and C33A cells. Endogenous and exogenous FAT1 was confirmed to interact with β-catenin, and the overexpression of β-catenin could partially block the effect of FAT1 on the proliferation, migration, and invasion of HeLa and C33A cells.
Indexed as
Identifiers
31933769PMC6949748W3003482803What 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.