ArticleToxicology research2024
Amentoflavone regulates the miR-124-3p/CAPN2 axis to promote mitochondrial autophagy in HCC cells.
Article in Toxicology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Enhancing GSDME-induced pyroptosis through low-dose doxorubicin/biflavonoid derivative co-loaded nanodisc in hepatocellular carcinoma.Drug delivery · 2025Article
- Traditional Chinese Medicine Monomers and Their Derivatives as a Promising Therapeutic Tool for Hepatocellular Carcinoma by Activation of Mitophagy.Drug design, development and therapy · 2025Review
- Targeting cell death mechanisms: the potential of autophagy and ferroptosis in hepatocellular carcinoma therapy.Frontiers in immunology · 2024Review
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Authors and funding
6 authors.
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Abstract
backgroundHepatocellular carcinoma (HCC) is a disease with poor prognosis and high mortality. Amentoflavone (AF) possesses the characteristics of marginal toxicity, stable curative effect, and good anti-HCC activity. This study aimed to evaluate the molecular mechanism of AF inhibiting HCC and provide a new idea for HCC treatment.
methodsClinical tissue of HCC was collected. AF was given with HCC cells, and transfected with corresponding vectors. MiR-124-3p expression in HCC clinical samples and cells was ascertained by qRT-PCR assay. HCC cells viability was identified by CCK-8 assay. LC3 protein expression was ascertained by immunofluorescence assay. The expressions of CAPN2, β-catenin and mitochondrial autophagy-related proteins were detected by western blot. Dual-luciferase reporter gene assay confirmed the targeting relationship of miR-124-3p and CAPN2.
resultsMiR-124-3p expression was inhibited and CAPN2 expression was increased in HCC tissues and cells. AF decreased HCC cell viability, up-regulated miR-124-3p expression, and inhibited CAPN2 expression and β-catenin nuclear transcription. Moreover, AF could activate the mitochondrial autophagy of HCC cells. MiR-124-3p specifically regulated CAPN2 expression. This study found that CAPN2 could promote β-catenin nuclear translocation, thus activating wnt/β-catenin pathway to inhibit mitochondrial autophagy in HCC cells. MiR-124-3p mimics enhanced AF function in promoting mitochondrial autophagy in HCC cells. However, CAPN2 overexpression, miR-124-3p inhibitor and SKL2001 attenuated the effectiveness of AF.
conclusionThis study confirmed that AF regulated miR-124-3p/CAPN2 axis to restraint β-catenin nuclear translocation and then inhibit the wnt/β-catenin pathway, thereby promoting mitochondrial autophagy in HCC.
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