ArticleScientific reports2017
The down-regulation of SLC7A11 enhances ROS induced P-gp over-expression and drug resistance in MCF-7 breast cancer cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 66 citations in OpenAlex.
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- Alterations of drug-resistant proteins in nasopharyngeal carcinoma after intensity-modulated radiation therapy with or without chemotherapy and correlation with clinicopathologic features and short-term prognosis.Discover oncology · 2025Article
- SLC7A11 Inhibitors Represent a Promising Therapeutic Target by Facilitating the Induction of Ferroptosis in Breast Cancer.International journal of molecular and cellular medicine · 2025Review
- The dual role of SLC7A11 in tumor drug resistance: mechanisms, challenges, and therapeutic potential.American journal of cancer research · 2025Review
- The amino acid transporter SLC7A11 expression in breast cancer.Cancer biology & therapy · 2024Article
- Hypoxia-induced BAP1 enhances erastin-induced ferroptosis in nasopharyngeal carcinoma by stabilizing H2A.Cancer cell international · 2024Article
- Impact of V9302, a Competitive Antagonist of Transmembrane Glutamine Flux on Reversal of Resistance in Breast Cancer Cell Lines.Pharmaceutics · 2024Article
- Article
- Amino acid transporters within the solute carrier superfamily: Underappreciated proteins and novel opportunities for cancer therapy.Molecular metabolism · 2024Review
- The superiority of PMFs on reversing drug resistance of colon cancer and the effect on aerobic glycolysis-ROS-autophagy signaling axis.Oncology research · 2024Article
- NFR2/ABC transporter axis in drug resistance of breast cancer cells.Molecular biology reports · 2023Review
- SLC7A11 as a Gateway of Metabolic Perturbation and Ferroptosis Vulnerability in Cancer.Antioxidants (Basel, Switzerland) · 2022Review
- A pH-responsive complex based on supramolecular organic framework for drug-resistant breast cancer therapy.Drug delivery · 2022Article
- A pH-responsive complex based on supramolecular organic framework for drug-resistant breast cancer therapy.Drug delivery · 2022Article
- The Role of SLC7A11 in Cancer: Friend or Foe?Cancers · 2022Review
- Chemosensitizing effect and mechanism of imperatorin on the anti-tumor activity of doxorubicin in tumor cells and transplantation tumor model.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Circ_0120175 promotes laryngeal squamous cell carcinoma development through up-regulating SLC7A11 by sponging miR-330-3p.Journal of molecular histology · 2022Article
- Influence of the Metabolism on Myeloid Cell Functions in Cancers: Clinical Perspectives.Cells · 2022Review
- Structural Characterization and Anti-breast Cancer ActivityFrontiers in nutrition · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adriamycin (ADR) induces the over-expression of P-glycoprotein (P-gp) and multiple drug resistance in breast cancer cells. However, the biochemical process and underlying mechanisms are not clear. Our previous study revealed that ADR increased reactive oxygen species (ROS) generation and decreased glutathione (GSH) biosynthesis, while N-acetylcysteine, the ROS scavenger, reversed the over-expression of P-gp. The present study showed that ADR inhibited the influx of cystine (the source material of GSH) and the activity of the SLC7A11 transporter (in charge of cystine uptake) in MCF-7 cells. For the first time, we showed that the down-regulation/silence of SLC7A11, or cystine deprivation, or enhanced ROS exposure significantly increased P-gp expression in MCF-7 cells. The down-regulation of SLC7A11 markedly enhanced ROS induced P-gp over-expression and drug resistance in MCF-7 cells; a combination of either an inhibited/silenced SLC7A11 or cystine deprivation and increased ROS dramatically promoted P-gp expression, which could be reversed by N-acetylcysteine. In contrast, the over-expression of SLC7A11, or supplementation with sufficiently cystine, or treatment with N-acetylcysteine significantly decreased P-gp expression and activity. It was suggested that ROS and SLC7A11/cystine were the two relevant factors responsible for the expression and function of P-gp, and that SLC7A11 might be a potential target modulating ADR resistance.
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