ArticleCancers2019
Targeting FAT1 Inhibits Carcinogenesis, Induces Oxidative Stress and Enhances Cisplatin Sensitivity through Deregulation of LRP5/WNT2/GSS Signaling Axis in Oral Squamous Cell Carcinoma.
Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- Roles of Wnt ligands and receptors in oral squamous cell carcinoma.Journal of Zhejiang University. Science. B · 2025Review
- Atypical cadherin FAT1 promotes tumorigenesis by suppressing autophagic cell death in glioblastoma under hypoxia or nutrient stress.Cellular & molecular biology letters · 2025Article
- mOncogene · 2025Article
- Immune factors and their role in tumor aggressiveness in glioblastoma: Atypical cadherin FAT1 as a promising target for combating immune evasion.Cellular & molecular biology letters · 2025Review
- Recent advances in the role of atypical cadherin FAT1 in tumorigenesis (Review).Oncology letters · 2025Review
- FAT1 knockdown enhances the CSC properties of HNSCC through p-CaMKII-mediated inactivation of the IFN pathway.International journal of biological sciences · 2025Article
- Integrating scRNA-seq and machine learning identifies MNAT1 as a therapeutic target in OSCC.Frontiers in immunology · 2025Article
- Connecting the dots: investigating the link between environmental, genetic, and epigenetic influences in metabolomic alterations in oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2024Review
- Targeting ferroptosis as a potential strategy to overcome the resistance of cisplatin in oral squamous cell carcinoma.Frontiers in pharmacology · 2024Review
- Review
- Genome-wide DNA methylation profiling of HPV-negative leukoplakia and gingivobuccal complex cancers.Clinical epigenetics · 2023Article
- The Potential of Liquid Biopsy in Detection of Endometrial Cancer Biomarkers: A Pilot Study.International journal of molecular sciences · 2023Article
- Tislelizumab plus nimotuzumab is effective against recurrent or metastatic oral squamous cell carcinoma among patients with a performance status score ≥ 2: a retrospective study.Frontiers in oncology · 2023Article
- Identification of causative gene mutation in an Iranian family with coloboma and nephropathy using whole exome sequencing.CEN case reports · 2022Article
- Somatic mutations in FAT cadherin family members constitute an underrecognized subtype of colorectal adenocarcinoma with unique clinicopathologic features.World journal of clinical oncology · 2022Article
- Analysis of senescence in gingival tissues and gingival fibroblast cultures.Clinical and experimental dental research · 2022Article
- Clinical significance of FAT1 gene mutation and mRNA expression in patients with head and neck squamous cell carcinoma.Molecular oncology · 2022Article
- Modulation of RNA splicing associated with Wnt signaling pathway using FD-895 and pladienolide B.Aging · 2022Article
- Genetic Alteration and Their Significance on Clinical Events in Small Cell Lung Cancer.Cancer management and research · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FAT atypical cadherin 1 (FAT1) regulates cell-cell adhesion and extracellular matrix architecture, while acting as tumor suppressor or oncogene, context-dependently. Despite implication of FAT1 in several malignancies, its role in oral squamous cell carcinoma (OSCC) remains unclear. Herein, we document the driver-oncogene role of FAT1, and its mediation of cell-death evasion, proliferation, oncogenicity, and chemoresistance in OSCC. In-silica analyses indicate FAT1 mutations are frequent and drive head-neck SCC, with enhanced expression defining high-risk population and poor prognosis. We demonstrated aberrant FAT1 mRNA and protein expression in OSCC compared with non-cancer tissues, whereas loss-of-FAT1-function attenuates human primary SAS and metastatic HSC-3 OSCC cell viability, without affecting normal primary human gingival fibroblast cells. shFAT1 suppressed PCNA and upregulated BAX/BCL2 ratio in SAS and HSC-3 cells. Moreover, compared with wild-type cells, shFAT1 concomitantly impaired HSC-3 cell migration, invasion, and clonogenicity. Interestingly, while over-expressed FAT1 characterized cisplatin-resistance (CispR), shFAT1 synchronously re-sensitized CispR cells to cisplatin, enhanced glutathione (GSH)/GSH synthetase (GSS)-mediated oxidative stress and deregulated LRP5/WNT2 signaling. Concisely, FAT1 is an actionable driver-oncogene in OSCC and targeting FAT1 in patients with erstwhile cisplatin-resistant OSCC is therapeutically promising.
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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.