ArticleBioMed research international2014
Emodin augments cisplatin cytotoxicity in platinum-resistant ovarian cancer cells via ROS-dependent MRP1 downregulation.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 60 citations in OpenAlex.
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- Activated PLK1 promotes the migration and invasion of polyploid giant cancer cells with daughter cells via β-catenin/STAT3 signaling pathway.Human cell · 2025Article
- Natural products for enhancing the sensitivity or decreasing the adverse effects of anticancer drugs through regulating the redox balance.Chinese medicine · 2024Review
- Small molecule targeted therapies for endometrial cancer: progress, challenges, and opportunities.RSC medicinal chemistry · 2024Review
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- A Review on Bioactive Anthraquinone and Derivatives as the Regulators for ROS.Molecules (Basel, Switzerland) · 2023Review
- Integrated clinical and metabolomic analysis of dengue infection shows molecular signatures associated with host-pathogen interaction in different phases of the disease.Metabolomics : Official journal of the Metabolomic Society · 2023Article
- Cisplatin in Ovarian Cancer Treatment-Known Limitations in Therapy Force New Solutions.International journal of molecular sciences · 2023Review
- Effect of thread depth and thread pitch on the primary stability of miniscrews receiving a torque load : A finite element analysis.Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie · 2023Article
- Evaluating complete surface-associated and secretory proteome of Leishmania donovani for discovering novel vaccines and diagnostic targets.Archives of microbiology · 2022Article
- Converting sounds to meaning with ventral semantic language networks: integration of interdisciplinary data on brain connectivity, direct electrical stimulation and clinical disconnection syndromes.Brain structure & function · 2022Review
- Alpinetin: A Review of Its Pharmacology and Pharmacokinetics.Frontiers in pharmacology · 2022Review
- Sporoderm-Broken Spores ofFrontiers in pharmacology · 2022Article
- Review
- Molecular mechanisms and cardiovascular implications of cancer therapy-induced senescence.Pharmacology & therapeutics · 2021Review
- Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies.Molecules (Basel, Switzerland) · 2021Review
- Emodin Induced Necroptosis and Inhibited Glycolysis in the Renal Cancer Cells by Enhancing ROS.Oxidative medicine and cellular longevity · 2021Article
- Amplification of oxidative stressNanoscale advances · 2020Article
- Emodin, a natural anthraquinone, suppresses liver cancer in vitro and in vivo by regulating VEGFRInvestigational new drugs · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intracellular level of reactive oxygen species (ROS) is closely associated with chemosensitivity of cancer cells. Overexpression of ATP binding cassette transporter MRP1 is correlated with resistance to platinum drugs. In this study, we tested the hypothesis that emodin, a potent ROS generator, may increase sensitivity of cisplatin-(cDDP-) resistant ovarian carcinoma cells to cDDP cytotoxicity via ROS-mediated suppression of MRP1 expression. Using the isogenic pair of the human ovarian carcinoma cell line COC1 and its cDDP resistant variant COC1/DDP, we found that ROS level in the cDDP-sensitive ovarian cancer cells was significantly higher than that in the cDDP-resistant cells. Emodin enhanced ROS production in COC1/DDP cells and consequently sensitized them to cDDP-induced apoptosis. These effects were reversed by addition of the antioxidant N-acetyl-L-cysteine (NAC). Cotreatment with emodin and cDDP inhibited the tumor growth in vivo by increasing tumor cell apoptosis. The emodin-enhanced cDDP cytotoxicity was attributable to downregulation of multidrug resistance-related protein 1 (MRP1) expression. Together, these results suggest that emodin could act as an adjunct to enhance the anticancer effect of cDDP likely through ROS-related downregulation of MRP1 expression, and may be of therapeutic potential in cDDP-refractory ovarian carcinomas.
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