ArticleThe American journal of pathology2012
Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
- A Transcriptomic Analysis of Cancer-Stromal Interactome in Lung Cancer Xenograft Models.Cancer science · 2026Article
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- Article
- Deciphering a cell death-associated signature for predicting prognosis and response to immunotherapy in lung squamous cell carcinoma.Respiratory research · 2023Article
- Fn14-Directed DART Nanoparticles Selectively Target Neoplastic Cells in Preclinical Models of Triple-Negative Breast Cancer Brain Metastasis.Molecular pharmaceutics · 2023Article
- High dimensionality reduction by matrix factorization for systems pharmacology.Briefings in bioinformatics · 2022Article
- Targeting fibroblast growth factor (FGF)-inducible 14 (Fn14) for tumor therapy.Frontiers in pharmacology · 2022Review
- Antibody-drug conjugates harboring a kinesin spindle protein inhibitor with immunostimulatory properties.Oncoimmunology · 2022Article
- Identification of Pan-Cancer Biomarkers Based on the Gene Expression Profiles of Cancer Cell Lines.Frontiers in cell and developmental biology · 2021Article
- In silico analysis of STX2a-PE15-P4A8 chimeric protein as a novel immunotoxin for cancer therapy.In silico pharmacology · 2021Article
- Mechanisms of drugs-resistance in small cell lung cancer: DNA-related, RNA-related, apoptosis-related, drug accumulation and metabolism procedure.Translational lung cancer research · 2020Review
- Aging-associated genesOncology letters · 2020Article
- Identification of aurintricarboxylic acid as a selective inhibitor of the TWEAK-Fn14 signaling pathway in glioblastoma cells.Oncotarget · 2017Article
- Enavatuzumab, a Humanized Anti-TWEAK Receptor Monoclonal Antibody, Exerts Antitumor Activity through Attracting and Activating Innate Immune Effector Cells.Journal of immunology research · 2017Article
- The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeutics.Oncogene · 2016Review
- Article
- The TWEAK Receptor Fn14 Is an Src-Inducible Protein and a Positive Regulator of Src-Driven Cell Invasion.Molecular cancer research : MCR · 2015Article
- Minimizing the non-specific binding of nanoparticles to the brain enables active targeting of Fn14-positive glioblastoma cells.Biomaterials · 2015Article
- FN14 expression correlates with MET in NSCLC and promotes MET-driven cell invasion.Clinical & experimental metastasis · 2014Article
- Mcl-1 mediates TWEAK/Fn14-induced non-small cell lung cancer survival and therapeutic response.Molecular cancer research : MCR · 2014Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Lung cancer is the leading cause of cancer deaths worldwide; approximately 85% of these cancers are non-small cell lung cancer (NSCLC). Patients with NSCLC frequently have tumors harboring somatic mutations in the epidermal growth factor receptor (EGFR) gene that cause constitutive receptor activation. These patients have the best clinical response to EGFR tyrosine kinase inhibitors (TKIs). Herein, we show that fibroblast growth factor-inducible 14 (Fn14; TNFRSF12A) is frequently overexpressed in NSCLC tumors, and Fn14 levels correlate with p-EGFR expression. We also report that NSCLC cell lines that contain EGFR-activating mutations show high levels of Fn14 protein expression. EGFR TKI treatment of EGFR-mutant HCC827 cells decreased Fn14 protein levels, whereas EGF stimulation of EGFR wild-type A549 cells transiently increased Fn14 expression. Furthermore, Fn14 is highly expressed in EGFR-mutant H1975 cells that also contain an EGFR TKI-resistance mutation, and high TKI doses are necessary to reduce Fn14 levels. Constructs encoding EGFRs with activating mutations induced Fn14 expression when expressed in rat lung epithelial cells. We also report that short hairpin RNA-mediated Fn14 knockdown reduced NSCLC cell migration and invasion in vitro. Finally, Fn14 overexpression enhanced NSCLC cell migration and invasion in vitro and increased experimental lung metastases in vivo. Thus, Fn14 may be a novel therapeutic target for patients with NSCLC, in particular for those with EGFR-driven tumors who have either primary or acquired resistance to EGFR TKIs.
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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.