ArticleOncology letters2022
Tepotinib suppresses proliferation, invasion, migration, and promotes apoptosis of melanoma cells via inhibiting MET and PI3K/AKT signaling pathways.
Article in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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
7 citing papers in PubMed, 5 citations in OpenAlex.
- Review
- Article
- Research progress of small molecule targeted drugs for non-small cell lung cancer.Frontiers in oncology · 2026Review
- Coptisine inhibits esophageal carcinoma growth by modulating pyroptosis via inhibition of HGF/c-Met signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- MET amplification correlates with poor prognosis and immunotherapy response as a subtype of melanoma: a multicenter retrospective study.BMC cancer · 2024Article
- Recent advances in the treatment of non-small cell lung cancer with MET inhibitors.Frontiers in chemistry · 2024Review
- Therapeutic targeting of anoikis resistance in cutaneous melanoma metastasis.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant melanoma seriously threatens public health and lowers the quality of life of the affected subjects. The present study was designed to explore the effects of tepotinib, a selective tyrosine kinase inhibitor of MET proto-oncogene, receptor tyrosine kinase (MET), on the progression of melanoma. Firstly, MTT assays were used to detect the proliferation of tepotinib-treated WM451 cells. The cell invasive and migratory activities were assessed using Transwell and wound healing assays, respectively. In addition, TUNEL staining was employed to determine cell apoptosis. Western blot analysis was utilized for the evaluation of the expression levels of apoptotic and epithelial-mesenchymal transition-related proteins, as well as of proteins involved in the PI3K/AKT signaling pathway. Subsequently, hepatocyte growth factor (HGF), a natural agonist of MET, was administered to WM451 cells to unravel the detailed mechanism of action of tepotinib in melanoma. The results indicated that the proliferation of WM451 cells was significantly decreased by tepotinib treatment. The inhibitory effects of tepotinib on the proliferation of WM451 cells occurred in a concentration-dependent manner. In addition, the migratory and invasive activities of WM451 cells were significantly suppressed following tepotinib treatment. It was also shown that tepotinib exhibited promotive effects on the induction of apoptosis of WM451 cells. Moreover, activation of MET and PI3K/AKT signaling pathways may be blocked by tepotinib treatment, whereas addition of HGF to the cells reversed the effects of tepotinib treatment on the malignant progression of WM451 cells. In conclusion, the data demonstrated that tepotinib suppressed the proliferation, invasion and migration of melanoma cells, whereas it could also induce their apoptosis. This evidence may provide a new perspective for the improvement of malignant melanoma.
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