ArticleThe Journal of clinical investigation2023
Aryl hydrocarbon receptor sulfenylation promotes glycogenolysis and rescues cancer chemoresistance.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- IDO1 regulating ROS rhythm reveals glycogenolysis/PPP as a cancer treatment target.Nature chemical biology · 2026Article
- Tryptophan metabolism in tumor microenvironment and therapeutic implications.Journal of advanced research · 2026Review
- The aryl hydrocarbon receptor inhibits antigen presentation to promote progression of pancreatic ductal adenocarcinoma.Journal of advanced research · 2026Article
- AhR-Siglec-15 axis regulates lysosomal Ca2+ release for sonic hedgehog medulloblastoma growth via TRPML1.Protein & cell · 2026Article
- Extracellular ATP promotes endocrine resistance in ER+ breast cancer through upregulation of PYGL.Cell death & disease · 2026Article
- Monophosphoryl lipid A boosts macrophage antimicrobial immunity by metabolically regulating source-specific ROS generation.Frontiers in immunology · 2026Article
- Review
- Oxidative stress in cancer: from tumor and microenvironment remodeling to therapeutic frontiers.Molecular cancer · 2025Review
- Oxidative Stress and Inflammation: Drivers of Tumorigenesis and Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2025Review
- Pharmacological potential of Chinese botanical drugs in managing chronic kidney disease by targeting mitochondrial quality control.Frontiers in pharmacology · 2025Review
- Circular RNAs modulate cancer drug resistance: advances and challenges.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- PCK1-mediated glycogenolysis facilitates ROS clearance and chemotherapy resistance in cervical cancer stem cells.Scientific reports · 2024Article
- The role of aryl hydrocarbon receptor in the occurrence and development of periodontitis.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevation of reactive oxygen species (ROS) levels is a general consequence of tumor cells' response to treatment and may cause tumor cell death. Mechanisms by which tumor cells clear fatal ROS, thereby rescuing redox balance and entering a chemoresistant state, remain unclear. Here, we show that cysteine sulfenylation by ROS confers on aryl hydrocarbon receptor (AHR) the ability to dissociate from the heat shock protein 90 complex but to bind to the PPP1R3 family member PPP1R3C of the glycogen complex in drug-treated tumor cells, thus activating glycogen phosphorylase to initiate glycogenolysis and the subsequent pentose phosphate pathway, leading to NADPH production for ROS clearance and chemoresistance formation. We found that basic ROS levels were higher in chemoresistant cells than in chemosensitive cells, guaranteeing the rapid induction of AHR sulfenylation for the clearance of excess ROS. These findings reveal that AHR can act as an ROS sensor to mediate chemoresistance, thus providing a potential strategy to reverse chemoresistance in patients with cancer.
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Registered trials
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