ArticleMolecular biomedicine2021
Role of novel cancer gene SLITRK3 to activate NTRK3 in squamous cell lung cancer.
Article in Molecular biomedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- iS2C2: a cointelligent platform for mechanistic discovery of disease cellular crosstalk.Signal transduction and targeted therapy · 2026Article
- Integrated transcriptomic and immune-associated network analysis of breast cancer patient-derived organoids reveals candidate inflammatory biomarkers.Frontiers in bioengineering and biotechnology · 2026Article
- Fibroblasts promote the progression of benign prostatic hyperplasia through colony-stimulating factor 1 receptor-mediated RTK signaling in prostatic epithelial cells.Molecular biomedicine · 2025Article
- Insight into the Association between Slitrk Protein and Neurodevelopmental and Neuropsychiatric Conditions.Biomolecules · 2024Review
- Human mutations inFrontiers in molecular neuroscience · 2024Article
- Systematic decoding the functional role of human endogenous retrovirus-derived RNAs in medulloblastoma.Neuro-oncology advancesArticle
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Authors and funding
8 authors.
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Abstract
The development of targeted therapies that inhibit cancer-driving oncogenes has improved outcomes of patients diagnosed with lung adenocarcinoma (LUAD). In contrast, patients diagnosed with lung squamous cell carcinoma (LUSC) suffer worse survival outcomes and lack effective targeted treatment options. Identification of molecular drivers of LUSC to support development of targeted treatments is urgently needed. Addressing this need, the current report introduces the novel cancer gene SLIT- and NTRK-like family member 3 (SLITRK3) and its role in activating the neurotrophic receptor tyrosine kinase 3 (NTRK3) in LUSC cells. Multiple genome-wide data sets from patient samples were produced by us or downloaded from public databases to analyze tumor gene copy number aberrations, mRNA expression and associated survival outcomes. An accompanying mechanistic study employed LUSC cell lines and multiple methods, including in situ immunofluorescence, sphere-formation assay, and fluorescence-activated cell sorting analysis of the CD133-positive cell fraction. Altogether, the results indicate that gene amplification and consequent high expression of SLITRK3 in LUSC is associated with worse outcomes and induces SLITRK3-dependent activation of NTRK3 to promote a cancer stem cell phenotype that is inhibited by existing NTRK-targeted inhibitors. Based on a recent literature search, this is the first report of a mechanistic role for SLITRK3 in cancer.
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