ArticleInternational journal of medical sciences2015
Artesunate Induces SKM-1 Cells Apoptosis by Inhibiting Hyperactive β-catenin Signaling Pathway.
Article in International journal of medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Artemisinin's molecular symphony: illuminating pathways for cancer therapy.Molecular biology reports · 2024Review
- HTINet2: herb-target prediction via knowledge graph embedding and residual-like graph neural network.Briefings in bioinformatics · 2024Article
- Transplant oncology and anti-cancer immunosuppressants.Frontiers in immunology · 2024Review
- Enhancing tumor photodynamic synergistic therapy efficacy through generation of carbon radicals by Prussian blue nanomedicine.Regenerative biomaterials · 2024Article
- Roles of ferroptosis in urologic malignancies.Cancer cell international · 2021Review
- Article
- Repurposing Artemisinin and its Derivatives as Anticancer Drugs: A Chance or Challenge?Frontiers in pharmacology · 2021Review
- Artemisinins as a novel anti-cancer therapy: Targeting a global cancer pandemic through drug repurposing.Pharmacology & therapeutics · 2020Review
- Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine.Chinese medicine · 2019Review
- Artesunate may inhibit liver fibrosis via the FAK/Akt/β-catenin pathway in LX-2 cells.BMC pharmacology & toxicology · 2018Article
- Artesunate induces apoptosis and autophagy in HCT116 colon cancer cells, and autophagy inhibition enhances the artesunate‑induced apoptosis.International journal of molecular medicine · 2018Article
- Artesunate-induced Cellular Effects Are Mediated by Specific EPH Receptors and Ephrin Ligands in Breast Carcinoma Cells.Cancer genomics & proteomicsArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionArtesunate (ART), a wildly used agent to treat severe malarial around the world, also has the power to inhibit growth of different types of tumor. However, the exact molecular mechanisms keep unknown.
methodIn this study, we used myelodysplastic syndrome (MDS) cells (SKM-1 cells) with differential ART concentrations treatment at multiple time points to observe the subsequence cell function alteration and the possible involved pathway genes.
resultsWe found that ART demonstrated the ability to inhibit proliferation and induce apoptosis in SKM-1 in a dose and time-dependent manner. Demethylase recovered CDH1 gene expression may be involved in the apoptosis process. The β-catenin protein translocated from the nucleus and cytoplasm to the membrane result in inactivation of β-catenin signaling pathway.
conclusionOur findings provide a rational basis to develop ART as a useful therapeutic agent for the treatment of myelodysplastic syndromes.
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