ArticlePloS one2017
Emodin reverses leukemia multidrug resistance by competitive inhibition and downregulation of P-glycoprotein.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Natural product-derived interventions for reversing multidrug resistance in resistant K562 leukemia cells: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Emodin and the Anthraquinone Scaffold: Therapeutic Promise and Strategies to Overcome Translational Barriers.Molecules (Basel, Switzerland) · 2026Review
- Medicinal plants as biological and socio-ecological components of One Health.Frontiers in pharmacology · 2026Review
- Natural Products Targeting BCR-ABL: A Plant-Based Approach to Chronic Myeloid Leukemia Treatment.Molecules (Basel, Switzerland) · 2025Review
- Review
- Recent Advances in Natural Products with Anti-Leukemia and Anti- Lymphoma Activities.Mini reviews in medicinal chemistry · 2024Review
- Mechanism of multidrug resistance to chemotherapy mediated by P‑glycoprotein (Review).International journal of oncology · 2023Review
- The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers.International journal of biological sciences · 2022Review
- The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb-A Summary Update.International journal of molecular sciences · 2021Review
- The Inhibitory Activity of Anthraquinones against Pathogenic Protozoa, Bacteria, and Fungi and the Relationship to Structure.Molecules (Basel, Switzerland) · 2020Article
- Effect ofPharmaceutics · 2020Article
- Emodin reverses 5-Fu resistance in human colorectal cancer via downregulation of PI3K/Akt signaling pathway.American journal of translational research · 2020Article
- Drug Bioavailability Enhancing Agents of Natural Origin (Bioenhancers) that Modulate Drug Membrane Permeation and Pre-Systemic Metabolism.Pharmaceutics · 2019Review
- Molecular Mechanism of Matrine fromBioMed research international · 2019Article
- Novel peptide myristoly-CM4 induces selective cytotoxicity in leukemia K562/MDR and Jurkat cells by necrosis and/or apoptosis pathway.Drug design, development and therapy · 2019Article
- Emodin inhibits pancreatic cancer EMT and invasion by up‑regulating microRNA‑1271.Molecular medicine reports · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development of multidrug resistance (MDR) is a continuous clinical challenge partially due to the overexpression of P-glycoprotein (P-gp) for chronic myelogenous leukemia (CML) patients. Herein, we evaluated the inhibitory potency of emodin, a natural anthraquinone derivative isolated from Rheum palmatum L, on P-gp in P-gp positive K562/ADM cells. Competition experiments combined with molecular docking analysis were utilized to investigate the binding modes between emodin and binding sites of P-gp. Emodin reversed adriamycin resistance in K562/ADM cells accompanied with the decrease of P-gp protein expression, further increasing the uptake of rhodamine123 in both K562/ADM and Caco-2 cells, indicating the inhibition of P-gp efflux function. Moreover, when incubated with emodin under different conditions where P-gp was inhibited, K562/ADM cells displayed increasing intracellular uptake of emodin, suggesting that emodin may be the potential substrate of P-gp. Importantly, rhodamine 123 could increase the Kintrinsic (Ki) value of emodin linearly, whereas, verapamil could not, implying that emodin competitively bound to the R site of P-gp and noncompetition existed between emodin and verapamil at the M site, in a good accordance with the results of molecular docking that emodin bound to the R site of P-gp with higher affinity. Based on our results, we suggest that emodin might be used to modulate P-gp function and expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.