ArticleMolecular cancer research : MCR2015
The TWEAK Receptor Fn14 Is an Src-Inducible Protein and a Positive Regulator of Src-Driven Cell Invasion.
Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 24 citations in OpenAlex.
- A Transcriptomic Analysis of Cancer-Stromal Interactome in Lung Cancer Xenograft Models.Cancer science · 2026Article
- Identification of a novel inflammatory mast cell subpopulation in triple-negative breast cancer.Frontiers in immunology · 2026Article
- Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast Cancer.Biology · 2025Article
- The Oncogenic Role of TNFRSF12A in Colorectal Cancer and Pan-Cancer Bioinformatics Analysis.Cancer research and treatment · 2025Article
- Impact of Targeting Moiety Type and Protein Corona Formation on the Uptake of Fn14-Targeted Nanoparticles by Cancer Cells.ACS nano · 2023Article
- Fn14-Directed DART Nanoparticles Selectively Target Neoplastic Cells in Preclinical Models of Triple-Negative Breast Cancer Brain Metastasis.Molecular pharmaceutics · 2023Article
- Lower Expression of TWEAK is Associated with Poor Survival and Dysregulate TIICs in Lung Adenocarcinoma.Disease markers · 2022Article
- Targeting fibroblast growth factor (FGF)-inducible 14 (Fn14) for tumor therapy.Frontiers in pharmacology · 2022Review
- Article
- Potential Molecular Mechanism of TNF Superfamily-Related Genes in Glioblastoma Multiforme Based on Transcriptome and Epigenome.Frontiers in neurology · 2021Article
- TNFRSF12A and a new prognostic model identified from methylation combined with expression profiles to predict overall survival in hepatocellular carcinoma.Translational cancer research · 2020Article
- Quercetin Inhibits the Proliferation and Metastasis of Human Non-Small Cell Lung Cancer Cell Line: The Key Role of Src-Mediated Fibroblast Growth Factor-Inducible 14 (Fn14)/ Nuclear Factor kappa B (NF-κB) pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- NETO2 promotes invasion and metastasis of gastric cancer cells via activation of PI3K/Akt/NF-κB/Snail axis and predicts outcome of the patients.Cell death & disease · 2019Article
- EGFRvIII-Stat5 Signaling Enhances Glioblastoma Cell Migration and Survival.Molecular cancer research : MCR · 2018Article
- Src Promotes Metastasis of Human Non-Small Cell Lung Cancer Cells through Fn14-Mediated NF-κB Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Fn14 Deficiency Ameliorates Anti-dsDNA IgG-Induced Glomerular Damage in SCID Mice.Journal of immunology research · 2018Article
- β1-Integrin Deletion From the Lens Activates Cellular Stress Responses Leading to Apoptosis and Fibrosis.Investigative ophthalmology & visual science · 2017Article
- Knockdown of the differentially expressed gene TNFRSF12A inhibits hepatocellular carcinoma cell proliferation and migration in vitro.Molecular medicine reports · 2017Article
- The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeutics.Oncogene · 2016Review
- Scavenger Receptors: Emerging Roles in Cancer Biology and Immunology.Advances in cancer research · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The TNF receptor superfamily member Fn14 (TNFRSF12A) is the sole signaling receptor for the proinflammatory cytokine TWEAK (TNFSF12). TWEAK: Fn14 engagement stimulates multiple signal transduction pathways, including the NF-κB pathway, and this triggers important cellular processes (e.g., growth, differentiation, migration, and invasion). The TWEAK-Fn14 axis is thought to be a major physiologic mediator of tissue repair after acute injury. Various studies have revealed that Fn14 is highly expressed in many solid tumor types, and that Fn14 signaling may play a role in tumor growth and metastasis. Previously, it was shown that Fn14 levels are frequently elevated in non-small cell lung cancer (NSCLC) tumors and cell lines that exhibit constitutive EGFR phosphorylation (activation). Furthermore, elevated Fn14 levels increased NSCLC cell invasion in vitro and lung metastatic tumor colonization in vivo. The present study reveals that EGFR-mutant NSCLC cells that express high levels of Fn14 exhibit constitutive activation of the cytoplasmic tyrosine kinase Src, and that treatment with the Src family kinase (SFK) inhibitor dasatinib decreases Fn14 gene expression at both the mRNA and protein levels. Importantly, siRNA-mediated depletion of the SFK member Src in NSCLC cells also decreases Fn14 expression. Finally, expression of the constitutively active v-Src oncoprotein in NIH 3T3 cells induces Fn14 gene expression, and NIH 3T3/v-Src cells require Fn14 expression for full invasive capacity. IMPLICATIONS: These results indicate that oncogenic Src may contribute to Fn14 overexpression in solid tumors, and that Src-mediated cell invasion could potentially be inhibited with Fn14-targeted therapeutics.
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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.