ArticleAmerican journal of translational research2026
Harmine suppresses the malignant phenotypes of Lewis lung carcinoma cells by inhibiting EGFR phosphorylation.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo investigate whether harmine (HM) suppresses the malignant phenotypes of Lewis lung carcinoma (LLC) cells through an epidermal growth factor receptor (EGFR) -mediated mechanism.
methodsPossible targets of HM and LLC-related genes were obtained from public databases, and overlapping targets were identified. A protein-protein interaction (PPI) network was constructed, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Molecular docking was performed to predict the binding mode of HM with EGFR. The expression of phosphorylated EGFR (p-EGFR) was examined in LLC cells.
resultsA total of 121 overlapping targets between HM and LLC were identified, and EGFR was recognized as a core hub target in the PPI network. Molecular docking predicted that HM could fit into the ATP-binding pocket of EGFR, with a binding energy below -7.0 kcal/mol. In LLC cells, HM showed selective cytotoxicity and significantly inhibited EGFR phosphorylation. HM also reduced cell proliferation, colony formation, migration, and invasion, while promoting apoptosis. These effects were partially reversed by EGFR overexpression.
conclusionHM suppresses the malignant phenotypes of LLC cells, at least in part, by inhibiting EGFR phosphorylation and EGFR-mediated signaling.
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