ArticleBMC cancer2022
Emodin inhibits invasion and migration of hepatocellular carcinoma cells via regulating autophagy-mediated degradation of snail and β-catenin.
Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Therapeutic Effects of Natural Products on Liver Cancer and Their Potential Mechanisms.Nutrients · 2024Pooled it
- Emodin Induces AIF-Associated Apoptosis and Suppresses Wnt/β-Catenin Signaling in Colorectal Cancer Stem-Like Cells.Biomolecules & therapeutics · 2026Article
- The power of phytochemicals in cancer chemoprevention through multi-target modulation of oncogenic signaling pathways.Discover oncology · 2026Review
- Mechanistic study of the role of emodin in targeting and inhibiting the Rap1 signaling pathway to regulate epithelial-mesenchymal transition and reverse cisplatin resistance in hepatocellular carcinoma.Translational cancer research · 2026Article
- Emodin: A Promising Natural Compound for Combating Fibrotic Diseases.Current medical science · 2026Review
- Plant secondary metabolites exert therapeutic effects by modulating autophagy pathways.Frontiers in plant science · 2026Review
- Research Progress on Quinone Compounds for the Treatment of Hepatocellular Carcinoma.Biomolecules · 2025Review
- Emodin promotes GSK-3β-mediated PD-L1 proteasomal degradation and enhances anti-tumor immunity in hepatocellular carcinoma.Chinese medicine · 2025Article
- Combining network pharmacology and RNA sequencing to reveal the mechanism of emodin for the treatment of human neuroblastoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Integrative network pharmacology and experimental validation reveal emodin derivatives as potential therapeutics for hepatocellular carcinoma.Journal of the Egyptian National Cancer Institute · 2025Article
- Chinese medicine monomers for hepatocellular carcinoma: New ideas related to autophagy.World journal of gastroenterology · 2025Review
- Aging-associated interleukin-11 drives the molecular mechanism and targeted therapy of idiopathic pulmonary fibrosis.European journal of medical research · 2025Review
- Natural anti-cancer products: insights from herbal medicine.Chinese medicine · 2025Review
- Success and Controversy of Natural Products as Therapeutic Modulators of Wnt Signaling and Its Interplay with Oxidative Stress: Comprehensive Review Across Compound Classes and Experimental Systems.Antioxidants (Basel, Switzerland) · 2025Review
- Role of emodin to prevent gastrointestinal cancers: recent trends and future prospective.Discover oncology · 2025Review
- Emodin reverses sorafenib resistance in hepatocellular carcinoma by inhibiting epithelial-mesenchymal transition via the Akt signaling pathway.Translational cancer research · 2025Article
- Natural Bioactive Compounds Targeting the Wnt/β-Catenin Pathway for the Treatment of Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Review
- Pharmacological and bioactive properties ofFrontiers in pharmacology · 2025Review
- The dual role of glycogen synthase kinase-3 beta (GSK3β) in neurodegenerative pathologies: interplay between autophagy and disease progression.Frontiers in pharmacology · 2025Review
- Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious studies reported that emodin extracted from Rheum palmatum L. exerts antiproliferation and antimetastatic effects in a variety of human cancer types. However, the role of emodin in hepatocellular carcinoma (HCC) remain unknown.
methodsEdU and colony formation assays were performed to evaluate the effects of emodin on proliferation. The mobility capacities of HCC treated with emodin were evaluated using wound healing assay. Transwell invasion and migration assays were performed to evaluate anti-migratory and anti-invasive effects of emodin on HCC. Annexin V-FITC/PI was performed to analyze the apoptosis. PI stain was performed to analyze cell cycle. RNA sequencing technology was used to identify the differentially expressed genes (DEGs) induced by emodin in HCC. The impact of emodin on autophagic flux in HepG2 cells was examined by mCherry-GFP-LC3 analysis. Western blot was used to assess the protein expressions of epithelial-mesenchymal transition (EMT), autophagy, PI3K/AKT/mTOR and Wnt/β-catenin signaling pathway.
resultsWe found that emodin inhibited the growth of HepG2 cells in a dose- and time-dependent manner. In addition, emodin inhibited cell proliferation, induced S and G2/M phases arrest, and promoted apoptosis in HepG2 cells. The migration and invasion of HepG2 cells were also suppressed by emodin. Enrichment analysis revealed that DEGs involved in cell adhesion, cancer metastasis and cell cycle arrest. Moreover, western bolt results show that emodin-induced autophagy promotes Snail and β-catenin degradation. We also found that blocking autophagic flux after emodin treatment caused EMT reversal. Furthermore, the PI3K agonist Y-P 740 significantly reversed the phosphorylation levels of GSK3β and mTOR. These results indicated that emodin induced autophagy and inhibited the EMT in part through suppression of the PI3K/AKT/mTOR and Wnt/β-catenin pathways.
conclusionOur study indicated that emodin inhibited cell metastasis in HCC via the crosstalk between autophagy and EMT.
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