ArticlePloS one2015
Fas Signaling Promotes Gastric Cancer Metastasis through STAT3-Dependent Upregulation of Fascin.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Gastric Cancer Organoids: Mechanistic Insights, Drug Discovery, and Translational Advances in Precision Medicine.Journal of gastric cancer · 2026Review
- Fascin-1: Updated biological functions and therapeutic implications in cancer biology.BBA advances · 2022Review
- Review
- Emerging Role of Fascin-1 in the Pathogenesis, Diagnosis, and Treatment of the Gastrointestinal Cancers.Cancers · 2021Review
- Fascin actin-bundling protein 1 in human cancer: promising biomarker or therapeutic target?Molecular therapy oncolytics · 2021Review
- miR-196b-5p-mediated downregulation of FAS promotes NSCLC progression by activating IL6-STAT3 signaling.Cell death & disease · 2020Article
- The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers.Nature reviews. Cancer · 2018Review
- Prognostic significance of microsatellite instability‑associated pathways and genes in gastric cancer.International journal of molecular medicine · 2018Article
- Fascin Induces Epithelial-Mesenchymal Transition of Cholangiocarcinoma Cells by Regulating Wnt/β-Catenin Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFas signaling-activated signal transducers and activators of transcription 3 (STAT3) is required for Fascin upregulation. As an actin-bundling protein, Fascin can mediate gastric cancer (GC) cell migration.
methodsGastric cancer AGS cells were treated with anti-Fas (5 μg/ml) for 2 h, in order to stimulate the activation of the Fas signaling. The in vitro migration of Fas signaling-activated AGS cells was assessed using Transwell chambers. The levels of Fascin and phosphorylated STAT3 were detected by Western blotting analyses. Nude mice were injected intravenously with AGS cells treated with anti-Fas or treated with STAT3 inhibitor without anti-Fas; tumor pulmonary metastases were measured. Fascin protein expression in tumor tissues was detected by immunohistochemistry. The Fas and Fascin mRNA levels in tumor tissues from patients with GC were measured by real-time PCR and their correlation was analyzed.
resultsThe activation of Fas signaling promoted cell migration and resulted in STAT3-dependent Fascin upregulation in AGS cells. STAT3 enhanced Fascin levels in vivo. Fascin was the mediator of Fas signaling-induced AGS cell migration in vitro and in vivo. Furthermore, there was a positive correlation between Fas and Fascin mRNA levels in tumor tissues from GC patients.
conclusionsFas signaling promotes GC metastasis through the STAT3/Fascin pathway, which may provide a new target for GC therapy.
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