ReviewOxidative medicine and cellular longevity2016
Redox Control of Multidrug Resistance and Its Possible Modulation by Antioxidants.
Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 74 citations in OpenAlex.
- Label-Free Proteomics Revealed Oxidative Stress and Inflammation as Factors That Enhance Chemoresistance in Luminal Breast Cancer.Oxidative medicine and cellular longevity · 2019Trial
- POU2F1 Promotes Chemoresistance in Colorectal Cancer Cells via Attenuates the MDR2 Degradation Mediated by PPP1R11 Lactylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Redox Homeostasis as a Therapeutic Target in Chronic Oxidative Diseases: Implications for Cancer Treatment.Antioxidants (Basel, Switzerland) · 2026Review
- Melatonin Overcomes Cancer Multidrug Resistance by Downregulating ABCB1 Expression and Modulating Mitochondrial Function.Journal of pineal research · 2025Article
- A comprehensive update on the potential of curcumin to enhance chemosensitivity in colorectal cancer.Pharmacological reports : PR · 2025Review
- The role and therapeutic potential of glucose metabolism in multidrug resistance of cancer.Frontiers in cell and developmental biology · 2025Review
- Tumor microenvironment targeted nano-drug delivery systems for multidrug resistant tumor therapy.Theranostics · 2025Review
- Epigenetic regulation of targeted ferroptosis: A new strategy for drug development.Journal of pharmaceutical analysis · 2024Review
- Natural products reverse cancer multidrug resistance.Frontiers in pharmacology · 2024Review
- Harnessing small extracellular vesicles for pro-oxidant delivery: novel approach for drug-sensitive and resistant cancer therapy.Journal of controlled release : official journal of the Controlled Release Society · 2024Article
- NADPH Oxidases: From Molecular Mechanisms to Current Inhibitors.Journal of medicinal chemistry · 2023Review
- Article
- The Alternating Access Mechanism in Mammalian Multidrug Resistance Transporters and Their Bacterial Homologs.Membranes · 2023Article
- Potential Nanotechnology-Based Therapeutics to Prevent Cancer Progression through TME Cell-Driven Populations.Pharmaceutics · 2022Review
- Emerging nanotechnology-based therapeutics to combat multidrug-resistant cancer.Journal of nanobiotechnology · 2022Review
- Verbascoside potentiates the effect of tyrosine kinase inhibitors on the induction of apoptosis and oxidative stress via the Abl-mediated MAPK signalling pathway in chronic myeloid leukaemia.Experimental and therapeutic medicine · 2022Article
- The Role of SLC7A11 in Cancer: Friend or Foe?Cancers · 2022Review
- Research Progress and Prospects of Autophagy in the Mechanism of Multidrug Resistance in Tumors.Journal of oncology · 2022Review
- Ferroptosis Induction in Multiple Myeloma Cells Triggers DNA Methylation and Histone Modification Changes Associated with Cellular Senescence.International journal of molecular sciences · 2021Article
- Effects of Heavy Isotopes (Sports (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinical efficacy of anticancer chemotherapies is dramatically hampered by multidrug resistance (MDR) dependent on inherited traits, acquired defence against toxins, and adaptive mechanisms mounting in tumours. There is overwhelming evidence that molecular events leading to MDR are regulated by redox mechanisms. For example, chemotherapeutics which overrun the first obstacle of redox-regulated cellular uptake channels (MDR1, MDR2, and MDR3) induce a concerted action of phase I/II metabolic enzymes with a temporal redox-regulated axis. This results in rapid metabolic transformation and elimination of a toxin. This metabolic axis is tightly interconnected with the inducible Nrf2-linked pathway, a key switch-on mechanism for upregulation of endogenous antioxidant enzymes and detoxifying systems. As a result, chemotherapeutics and cytotoxic by-products of their metabolism (ROS, hydroperoxides, and aldehydes) are inactivated and MDR occurs. On the other hand, tumour cells are capable of mounting an adaptive antioxidant response against ROS produced by chemotherapeutics and host immune cells. The multiple redox-dependent mechanisms involved in MDR prompted suggesting redox-active drugs (antioxidants and prooxidants) or inhibitors of inducible antioxidant defence as a novel approach to diminish MDR. Pitfalls and progress in this direction are discussed.
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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.