Potential targets and molecular mechanisms of curcumin in treating Laryngeal and Pharyngeal Carcinoma throat cancer based on network pharmacology and bioinformatics analysis.

Authors

Jixiang Lei, Xianyun Tang, Yuanchao Lin, Rui Yang, Zhiyue Ma

Published in

Mutation research. Volume 833. Pages 111943. Jul 13, 2026. Epub Jul 13, 2026.

Abstract

Curcumin exhibits significant antitumor activity, inhibiting proliferation, angiogenesis, invasion, and metastasis, highlighting its potential for cancer treatment. However, its mechanisms in Laryngeal and Pharyngeal Carcinoma remain unclear. Therefore, this study aims to elucidate these mechanisms through in vitro and in vivo experiments.
Cell functions were examined using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), 5-Ethynyl-2'-deoxyuridine (EdU) staining, tube formation assay, flow cytometry, and Transwell assays. Laryngeal and Pharyngeal Carcinoma-related genes were screened using GeneCards database, while curcumin-related genes were predicted using TCMSP and Swiss Target Prediction databases. Enrichment analysis of overlapping genes was performed using KEGG and GO analysis. Additionally, the core genes from common target genes were analyzed using Cytoscape and its plugins Cytohubba and MCODE. Gene expression was detected using reverse transcription-quantitative polymerase chain reaction (qRT-PCR) and western blot. Molecular docking was used to computationally predict the binding affinity between curcumin and EP300, followed by normal mode analysis (NMA)-based simulation to hypothetically explore complex stability under equilibrium conditions as a static approximation. Xenograft tumor models were constructed to investigate the role of curcumin and EP300.
Curcumin suppressed Laryngeal and Pharyngeal Carcinoma cell proliferation, migration, and invasion, and HUVEC tube formation, and promoted cancer cell apoptosis. Six of the eight curcumin-targeted genes were overexpressed in Laryngeal cancer (in both datasets), with NFE2L2 non-significantly upregulated and BCL2 showing heterogeneous expression. EP300 expression was increased in Laryngeal and Pharyngeal Carcinoma tissues and cells, and curcumin inhibited EP300 expression. Molecular docking, coupled with NMA, predicted favorable binding affinity and suggested that the curcumin and EP300 histone acetyltransferase (HAT) domain complex forms a stable binding mode. Notably, curcumin suppressed Laryngeal and Pharyngeal Carcinoma cell proliferation, migration, invasion, and HUVEC tube formation, and promoted cancer cell apoptosis in a process involving EP300, as demonstrated by rescue experiments with EP300 overexpression. In addition, EP300 overexpression reversed the inhibitory effect of curcumin on tumor growth.
Curcumin inhibits FaDu and AMC-HN-8 cell proliferation, HUVEC tube formation, cancer cell migration, and invasion and promotes cell apoptosis in a process involving EP300, as demonstrated by EP300 overexpression rescue experiments.

PMID:
42468085
Bibliographic data and abstract were imported from PubMed on 18 Jul 2026.

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