ArticleCancer & metabolism2021
Sulfasalazine modifies metabolic profiles and enhances cisplatin chemosensitivity on cholangiocarcinoma cells in in vitro and in vivo models.
Article in Cancer & metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Amino acid metabolic reprogramming: future prospects for cholangiocarcinoma therapy.Cell death discovery · 2026Review
- Systems biology insights into the molecular drivers of childhood stunting and implications for intervention.Frontiers in nutrition · 2026Review
- The evolving landscape of cancer cachexia prevention: A review of metronomic chemotherapy and drug repurposing strategies.Medical oncology (Northwood, London, England) · 2025Review
- Exploring Emerging Therapeutic Targets in Osteosarcoma by Revisiting the Immune and Cancer-Intrinsic Hallmarks of Cancer.Cancers · 2025Review
- Glutathione-associated redox regulation alleviates radio-resistance of canine cancer stem-like cells with low proteasome activity.Scientific reports · 2025Article
- Demystifying metabolic‒immune crosstalk: how amino acid metabolic reprogramming shapes the malignant phenotype and macrophage polarization of biliary and pancreatic tumors.International journal of biological sciences · 2025Review
- CD44 variant exons induce chemoresistance by modulating cell death pathways.Frontiers in cell and developmental biology · 2025Review
- Oncogenic accumulation of cysteine promotes cancer cell proliferation by regulating the translation of D-type cyclins.The Journal of biological chemistry · 2024Article
- Anti-CD44 Variant 10 Monoclonal Antibody Exerts Antitumor Activity in Mouse Xenograft Models of Oral Squamous Cell Carcinomas.International journal of molecular sciences · 2024Article
- Article
- Targeted Single-cell Isolation of Spontaneously Escaping Live Melanoma Cells for Comparative Transcriptomics.Cancer research communications · 2023Article
- Inhibition of lung adenocarcinoma by combinations of sulfasalazine (SAS) and disulfiram-copper (DSF-Cu) in cell line models and mice.Carcinogenesis · 2023Article
- A Novel Anti-CD44 Variant 9 Monoclonal Antibody CCurrent issues in molecular biology · 2023Article
- The impact of hypoxia and oxidative stress on proteo-metabolomic alterations of 3D cholangiocarcinoma models.Scientific reports · 2023Article
- Effect of M2-like macrophages of the injured-kidney cortex on kidney cancer progression.Cell death discovery · 2022Article
- Glutamatergic system components as potential biomarkers and therapeutic targets in cancer in non-neural organs.Frontiers in endocrinology · 2022Review
- High Levels of Serum IgG forInternational journal of general medicine · 2021Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundSulfasalazine (SSZ) is widely known as an xCT inhibitor suppressing CD44v9-expressed cancer stem-like cells (CSCs) being related to redox regulation. Cholangiocarcinoma (CCA) has a high recurrence rate and no effective chemotherapy. A recent report revealed high levels of CD44v9-positive cells in CCA patients. Therefore, a combination of drugs could prove a suitable strategy for CCA treatment via individual metabolic profiling.
methodsWe examined the effect of xCT-targeted CD44v9-CSCs using sulfasalazine combined with cisplatin (CIS) or gemcitabine in CCA in vitro and in vivo models and did NMR-based metabolomics analysis of xenograft mice tumor tissues.
resultsOur findings suggest that combined SSZ and CIS leads to a higher inhibition of cell proliferation and induction of cell death than CIS alone in both in vitro and in vivo models. Xenograft mice showed that the CD44v9-CSC marker and CK-19-CCA proliferative marker were reduced in the combination treatment. Interestingly, different metabolic signatures and significant metabolites were observed in the drug-treated group compared with the control group that revealed the cancer suppression mechanisms.
conclusionsSSZ could improve CCA therapy by sensitization to CIS through killing CD44v9-positive cells and modifying the metabolic pathways, in particular tryptophan degradation (i.e., kynurenine pathway, serotonin pathway) and nucleic acid metabolism.
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