ArticleBMC cancer2025
Quercetin affects apoptosis and autophagy in pediatric acute myeloid leukaemia cells by inhibiting PI3K/AKT signaling pathway activation through regulation of miR-224-3p/PTEN axis.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Quercetin attenuates deoxynivalenol-induced muscle developmental disorders in broilers by modulating the PI3K/Akt/mTOR pathway and reducing apoptosis.Poultry science · 2026Article
- Integrating UHPLC-Q-TOF-MS, Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulations to Reveal the Potential Mechanisms of Yiguanjian Decoction in Treating Liver Cancer.Chemistry & biodiversity · 2026Article
- Plant Bioactive Compounds at the Interface of Extraction Science, Green Nanoparticles and Applied Biotechnology: A Narrative Review.Molecules (Basel, Switzerland) · 2026Review
- Investigating the Mechanisms ofACS omega · 2026Article
- Review
- Quercetin and hematological cancers: where are we and where are we going?Molecular biology reports · 2025Review
- Modulation of Oxidative Stress in Diabetic Retinopathy: Therapeutic Role of Natural Polyphenols.Antioxidants (Basel, Switzerland) · 2025Review
- Synergistic Anti-Tumor Effects of Sulfatinib and Kaempferol on Pancreatic Neuroendocrine Tumors via CALCA-mediated PI3K/AKT/mTOR Pathway.International journal of biological sciences · 2025Article
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4 authors.
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Abstract
objectiveThe aim of this study was to investigate the mechanism by which quercetin (Que) affects apoptosis and autophagy in pediatric acute myeloid leukaemia (AML) cells by inhibiting the activation of the PI3K/AKT signaling pathway through the regulation of the miR-224-3p/PTEN axis.
methodsBlood samples were collected from AML children and healthy volunteers. miR-224-3p and PTEN expression levels were measured. AML cells were pre-treated with Que. MiR-224-3p and PTEN expression levels in AML cells were altered via plasmid transfection. After intervention, PI3K/AKT phosphorylation, AML cell proliferation and apoptosis, concentrations of interleukin-1 β (IL-1β) and tumor necrosis factor-α (TNF-α) in AML cell culture supernatant, apoptosis-related genes Bax and Bcl-2, and autophagy markers LC3-I and LC3-II were tested. The targeting relationship between miR-224-3p and PTEN was identified.
resultsMiR-224-3p expression was elevated in AML children, while PTEN was decreased. Que was available to accelerate AML cell apoptosis and restrain its autophagy. Que inhibited miR-224-3p expression and promoted PTEN expression. Upregulating miR-224-3p or downregulating PTEN weakened the effect of Que on AML cell apoptosis and autophagy. MiR-224-3p negatively modulated PTEN expression. Up-regulation of PTEN reversed the effects of up-regulation of miR-224-3p on apoptosis and autophagy in AML cells. In addition, Que inhibited PI3K/AKT signaling pathway activation, while up-regulation of miR-224-3p or down-regulation of PTEN could attenuate the inhibitory effect of Que on PI3K/AKT signaling pathway. Moreover, up-regulation of PTEN reversed the effect of up-regulation of miR-224-3p on the PI3K/AKT signaling pathway.
conclusionQue affects apoptosis and autophagy in pediatric AML cells by inhibiting PI3K/AKT signaling pathway activation through regulation of miR-224-3p/PTEN axis.
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