ArticleThe Journal of clinical investigation2013
MERTK receptor tyrosine kinase is a therapeutic target in melanoma.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 1 of them a synthesis that pooled it.
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Who cites it
100 citing papers in PubMed, 1 synthesis or guideline pooled it, 144 citations in OpenAlex.
- Identification of key genes in osteosarcoma by meta‑analysis of gene expression microarray.Molecular medicine reports · 2019Pooled it
- Preclinical evaluation of CPL423: a novel potent small-molecule inhibitor of TAM family and FLT3 kinase for cancer therapy.Frontiers in pharmacology · 2026Article
- The Crosstalk Between Efferocytosis and Macrophage Polarization in Diabetic Wounds: A Comprehensive Review.Journal of inflammation research · 2026Review
- STK38 Kinase Promotes Cell Migration Induced by Oncogenic Ras via MerTK Activation.International journal of molecular sciences · 2025Article
- Structure-Based Design of Potent and Selective MerTK Inhibitors by Modulating the Conformation of αC Helix.Journal of medicinal chemistry · 2025Article
- Targeting Frequent Efferocytosis in Tumor Microenvironment is a New Direction for Cancer Treatment.Small science · 2025Review
- Survival expectations in melanoma patients: a molecular prognostic model associated with aging.Discover oncology · 2025Article
- Targeting MERTK tyrosine kinase: Virtual screening and molecular dynamics insights for anti-cancer drug development.PloS one · 2025Article
- MERTK Inhibition as a Targeted Novel Cancer Therapy.International journal of molecular sciences · 2024Review
- Establishment of a novel efferocytosis potential index predicts prognosis and immunotherapy response in cancers.Heliyon · 2024Article
- MerTK Drives Proliferation and Metastatic Potential in Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Targeting the receptor tyrosine kinase MerTK shows therapeutic value in gastric adenocarcinoma.Cancer medicine · 2024Article
- GAS6/TAM Axis as Therapeutic Target in Liver Diseases.Seminars in liver disease · 2024Article
- Novel Substrate Prediction for the TAM Family of RTKs Using Phosphoproteomics and Structure-Based Modeling.ACS chemical biology · 2024Article
- Design, Synthesis, and Biological Evaluation of 2-Substituted Aniline Pyrimidine Derivatives as Potent Dual Mer/c-Met Inhibitors.Molecules (Basel, Switzerland) · 2024Article
- Review
- Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations.Cancers · 2023Article
- TAM family kinases as therapeutic targets at the interface of cancer and immunity.Nature reviews. Clinical oncology · 2023Review
- PCSK9 facilitates melanoma pathogenesis via a network regulating tumor immunity.Journal of experimental & clinical cancer research : CR · 2023Article
- N-glycosylation stabilizes MerTK and promotes hepatocellular carcinoma tumor growth.Redox biology · 2022Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 8 institutions in 2 countries.
Funding
Abstract
Metastatic melanoma is one of the most aggressive forms of cutaneous cancers. Although recent therapeutic advances have prolonged patient survival, the prognosis remains dismal. C-MER proto-oncogene tyrosine kinase (MERTK) is a receptor tyrosine kinase with oncogenic properties that is often overexpressed or activated in various malignancies. Using both protein immunohistochemistry and microarray analyses, we demonstrate that MERTK expression correlates with disease progression. MERTK expression was highest in metastatic melanomas, followed by primary melanomas, while the lowest expression was observed in nevi. Additionally, over half of melanoma cell lines overexpressed MERTK compared with normal human melanocytes; however, overexpression did not correlate with mutations in BRAF or RAS. Stimulation of melanoma cells with the MERTK ligand GAS6 resulted in the activation of several downstream signaling pathways including MAPK/ERK, PI3K/AKT, and JAK/STAT. MERTK inhibition via shRNA reduced MERTK-mediated downstream signaling, reduced colony formation by up to 59%, and diminished tumor volume by 60% in a human melanoma murine xenograft model. Treatment of melanoma cells with UNC1062, a novel MERTK-selective small-molecule tyrosine kinase inhibitor, reduced activation of MERTK-mediated downstream signaling, induced apoptosis in culture, reduced colony formation in soft agar, and inhibited invasion of melanoma cells. This work establishes MERTK as a therapeutic target in melanoma and provides a rationale for the continued development of MERTK-targeted therapies.
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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.