ArticleMolecular biology reports2024
Cyproheptadine inhibits in vitro and in vivo lung metastasis and drives metabolic rewiring.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Reprogrammed MDSCs promote Th1-dominant antitumour response via CD40 induced by autocrine TNF-α after combining cryo-thermal therapy with IL6 and IL17A neutralization.Clinical and translational medicine · 2025Article
- Repurposing serotonergic drugs for gastric cancer: induction of apoptosis in vitro.Molecular biology reports · 2025Article
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
- Synergistic Anti-Cancer Effects of Curcumin and Thymoquinone Against Melanoma.Antioxidants (Basel, Switzerland) · 2024Article
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9 authors.
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Abstract
backgroundNon-small cell lung cancer (NSCLC) accounts for 81% of lung cancer cases, among which over 47% presented with distant metastasis at the time of diagnosis. Despite the introduction of targeted therapy and immunotherapy, enhancing the survival rate and overcoming the development of resistance remain a big challenge. Thus, it is crucial to find potential new therapeutics and targets that can mitigate lung metastasis and investigate its effects on biomarkers, such as cellular metabolomics. In the current study, we investigated the role of cyproheptadine (CPH), an FDA-approved anti-histamine drug in lung metastasis in vitro and in vivo. METHODS AND
resultsCPH showed potent cytotoxicity on different lung cancer cell lines in vitro. Moreover, CPH decreased invasion and migration of LLC1 and A549 cells in Matrigel invasion transwell and plate scratch assays. The in vivo LLC1 syngeneic lung cancer model found decreased number of metastatic nodules on the surface of lungs of Setd7 KO mice compared to SETD7 WT. CPH treatment resulted in decreased growth of LLC1 subcutaneous tumors compared to untreated SETD7 WT. Finally, metabolomic study of tumor tissues showed rewiring of metabolomic pathways and downregulation of amino acids, such as arginine, serine, and glycine) in Setd7 KO and WT treated with CPH compared to untreated Setd7 WT mice.
conclusionThese findings identify CPH as a potential therapeutic agent to block metastasis in advanced NSCLC and suggest SETD7 as a potential target for the prevention of lung metastasis.
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