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Mechanism of Nitidine chloride against esophageal squamous carcinoma based on network pharmacology, molecular docking, and experimental validation
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DOI：10.1007/s12672-026-05701-x.png)
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Abstract
En 中文
Nitidine chloride (NC) is a natural alkaloid that inhibits tumor proliferation and induces apoptosis in tumor cells. However, the role of NC in esophageal squamous cell carcinoma (ESCC) remains unclear. We aimed to explore the effects of NC on the proliferation, apoptosis, and migration of ESCC cells and the mechanisms thereof. Network pharmacology and bioinformatics approaches were employed to construct compound-target and protein–protein interaction networks, enabling the identification of pivotal therapeutic targets. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway enrichment analyses were performed. Molecular docking was performed using the AutoDock software. Finally, in vitro and in vivo experiments validated the anti-tumor effects and underlying mechanisms of NC. Network pharmacology identified NC as a multitarget agent against ESCC, and GO/KEGG analyses identified the MAPK pathway as a key hub. Strong binding affinities between NC and MAPK molecules were confirmed by molecular docking. The functional experiments demonstrated that in both cell and animal models, NC inhibited the growth of ESCC and induced apoptosis, highlighting its possible mechanism of action through the activation of ROS to inhibit the MAPK pathway. NC may serve as potential adjuvant therapeutic agents for ESCC treatment. Although we demonstrated significant anti-ESCC efficacy, its safety profile requires further evaluation through systematic toxicological studies and pharmacokinetic analyses. This is a critical prerequisite for its development as a clinical anticancer drug.
Keywords:
Nitidine chloride
MAPK
Esophageal squamous cell carcinoma
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