Investigating the Mechanisms of against Acute Lymphoblastic Leukemia through Network Pharmacology and Experimental Validation.
1/5 보강
[OBJECTIVE] This study investigates the underlying mechanisms of on apoptosis in acute lymphoblastic leukemia (ALL) cells using an integrated approach that combines network pharmacology, molecular do
APA
Xu X, Zhou S, et al. (2026). Investigating the Mechanisms of against Acute Lymphoblastic Leukemia through Network Pharmacology and Experimental Validation.. ACS omega, 11(5), 7756-7768. https://doi.org/10.1021/acsomega.5c09488
MLA
Xu X, et al.. "Investigating the Mechanisms of against Acute Lymphoblastic Leukemia through Network Pharmacology and Experimental Validation.." ACS omega, vol. 11, no. 5, 2026, pp. 7756-7768.
PMID
41696298 ↗
Abstract 한글 요약
[OBJECTIVE] This study investigates the underlying mechanisms of on apoptosis in acute lymphoblastic leukemia (ALL) cells using an integrated approach that combines network pharmacology, molecular docking, and cellular experiments.
[METHODS] Active ingredients of and their potential targets were obtained from public databases, along with target genes associated with ALL. Intersecting targets were identified and analyzed through protein-protein interaction (PPI) network analysis to screen for hub genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses are conducted on the common targets. A network linking , its active components, targets, and KEGG pathways is constructed to identify key bioactive components. Molecular docking is performed to assess the binding affinities between the active compounds and core targets. Finally, in vitro experiments validate the predictions derived from network pharmacology.
[RESULTS] PPI analysis identified five hub genes of against ALL: CASP3, TNF, IL6, TP53, and AKT1. GO and KEGG analyses reveal that the mechanisms primarily involve the regulation of apoptotic signaling pathways, Bcl-2 family protein complexes, the PI3K/AKT and p53 pathway. Network analysis indicates that quercetin acts as a central active component of against ALL. Molecular docking revealed potent binding affinities of quercetin toward all five core targets. Cellular experiments further confirm that quercetin inhibits the proliferation of ALL cells and induces mitochondrial pathway-mediated apoptosis, potentially through the modulation of the PI3K/AKT and p53 pathways.
[CONCLUSION] This study reveals that quercetin, a key active ingredient of , mediates its anti-ALL activity by modulating the PI3K/AKT/p53 axis while inducing mitochondrial apoptosis. These findings provide reliable experimental evidence for utilizing in the treatment of ALL.
[METHODS] Active ingredients of and their potential targets were obtained from public databases, along with target genes associated with ALL. Intersecting targets were identified and analyzed through protein-protein interaction (PPI) network analysis to screen for hub genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses are conducted on the common targets. A network linking , its active components, targets, and KEGG pathways is constructed to identify key bioactive components. Molecular docking is performed to assess the binding affinities between the active compounds and core targets. Finally, in vitro experiments validate the predictions derived from network pharmacology.
[RESULTS] PPI analysis identified five hub genes of against ALL: CASP3, TNF, IL6, TP53, and AKT1. GO and KEGG analyses reveal that the mechanisms primarily involve the regulation of apoptotic signaling pathways, Bcl-2 family protein complexes, the PI3K/AKT and p53 pathway. Network analysis indicates that quercetin acts as a central active component of against ALL. Molecular docking revealed potent binding affinities of quercetin toward all five core targets. Cellular experiments further confirm that quercetin inhibits the proliferation of ALL cells and induces mitochondrial pathway-mediated apoptosis, potentially through the modulation of the PI3K/AKT and p53 pathways.
[CONCLUSION] This study reveals that quercetin, a key active ingredient of , mediates its anti-ALL activity by modulating the PI3K/AKT/p53 axis while inducing mitochondrial apoptosis. These findings provide reliable experimental evidence for utilizing in the treatment of ALL.
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