Exploration on the mechanism of curcumin in intervening leukemia based on transcriptomics and network pharmacology
10.3760/cma.j.cn431274-20240826-01317
- VernacularTitle:基于转录组学与网络药理学探讨姜黄素干预白血病的作用机制
- Author:
Guangzhi YU
1
;
Na LI
;
Zongxuan HUANG
;
Sen WANG
;
Fengyun DONG
Author Information
1. 济宁医学院附属医院儿科，济宁 272000
- Publication Type:Journal Article
- Keywords:
Leukemia;
Transcriptome;
Network pharmacology;
Curcumin
- From:
Journal of Chinese Physician
2025;27(8):1162-1166
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the mechanism of curcumin (Cur) in intervening leukemia based on transcriptomics and network pharmacology.Methods:(1) Cell proliferation experiment: Leukemia MV-4-11 cells were cultured in vitro and divided into the control group (DMSO), 15 μmol/L curcumin group (Cur 15 μmol/L), and 20 μmol/L curcumin group (Cur 20 μmol/L). The CFSE method by flow cytometry was used to determine the inhibitory effect of curcumin on the growth of leukemia MV-4-11 cells at 0, 24, and 48 hours. (2) Network pharmacology analysis: the Smiles number of curcumin was obtained using the PubChem database. The targets of curcumin were retrieved from SwissTargetPrediction, SEA, TTD, and CTD platforms. Leukemia-related targets were screened using Genecards, OMIM, TTD, and CTD databases, and the intersection targets of curcumin-leukemia were further collected. (3) Transcriptomics and network pharmacology analysis: RNA from MV-4-11 cells in the control group and Cur group was collected, transcriptome sequencing was performed, and the common targets of differential genes in network pharmacology and transcriptomics were collected. The STRING website and Cytoscape software were used to construct a protein-protein interaction (PPI) network for the intersection targets. The David database and micro-bioinformatics were used for enrichment analysis based on gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Finally, the core targets and main pathways of curcumin in anti-leukemia were screened out.Results:(1) Compared with the control group, 15 μmol/L and 20 μmol/L curcumin significantly inhibited the proliferation of MV-4-11 cells (all P<0.05). (2) Network pharmacology analysis showed 1 209 curcumin drug targets and 7 702 leukemia-related targets, with 901 intersection targets for curcumin′s anti-leukemia effect. (3) Transcriptome sequencing showed 14 714 genes expressed in the curcumin group and 13 689 genes in the control group, with a total of 3 064 differentially expressed genes, including 2 189 up-regulated genes and 875 down-regulated genes. There were 182 intersection targets between network pharmacology and transcriptomics. KEGG enrichment results indicated that the anti-leukemia targets of curcumin were mainly related to cancer signaling pathways, phosphatidylinositol-3-kinase signaling pathway (PI3K-Akt) signaling pathway, and mitogen-activated protein kinase (MAPK) signaling pathway. Conclusions:This study obtained the gene expression profile of curcumin acting on leukemia and elaborated the molecular mechanism of inhibiting leukemia cell proliferation, which is mainly involved in cancer signaling pathways, PI3K-Akt signaling pathway, MAPK signaling pathway, etc., indicating that the inhibitory effect of curcumin on leukemia is multi-faceted and multi-level.
