BACKGROUND Nasopharyngeal carcinoma (NPC) is publicly known as a malignant tumor. Our previous study reports plumbagin exhibiting potent anti-cancer actions. Howbeit, more mechanical details of plumbagin against NPC remain untapped.… Click to show full abstract
BACKGROUND Nasopharyngeal carcinoma (NPC) is publicly known as a malignant tumor. Our previous study reports plumbagin exhibiting potent anti-cancer actions. Howbeit, more mechanical details of plumbagin against NPC remain untapped. Here, our study aimed to unmask core targets/genes and anti-NPC mechanisms involved signaling pathways of plumbagin prior to being validated biochemically. METHODS Network pharmacology approach was employed to respective identification of mutual and core targets/genes in plumbagin and/treating NPC. Molecular docking determination was used to identify core target proteins for biochemical validation through using human and cell line samples. RESULTS Total 60 anti-NPC genes of plumbagin were screened out, and then 9 core target genes of plumbagin against NPC were identified accordingly. The enrichment findings revealed detailed biological functions and pharmacological pathways of plumbagin against NPC. Moreover, in-silico analysis using molecular docking had determined the core targets for further experimental validation, comprising protein kinase B (AKT1), sarcoma gene (SRC). In human sample validation, clinical NPC sections showed increased positive expressions of AKT1, SRC. Additionally, plumbagin-treated NPC cells resulted in inactivated protein expressions of AKT1, SRC. CONCLUSIONS The re-identified core targets/genes in molecular docking report may be functioned as plumbagin-related pharmacological targets for treating NPC via experimental validation. Furthermore, additional anti-NPC molecular mechanisms of plumbagin action were disclosed on the basis of enrichment findings. This article is protected by copyright. All rights reserved.
               
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