ArticleThe Biochemical journal2022
Carbidopa, an activator of aryl hydrocarbon receptor, suppresses IDO1 expression in pancreatic cancer and decreases tumor growth.
Article in The Biochemical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.
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Who cites it
10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.
- Repurposing neurological drugs for brain cancer therapeutics: A systematic approach to identify charged molecules for affinity-based local drug delivery systems.International journal of pharmaceutics · 2025Pooled it
- Gut microbiota metabolites in the immunoregulation of enteritis: research progress.Frontiers in immunology · 2025Pooled it
- Drug Repurposing in Oncology: A Strategic Pathway to Unlocking New Therapeutic Potential.Therapeutic innovation & regulatory science · 2026Review
- Role of Tryptophan Metabolism in Cancer.Cancer innovation · 2025Review
- The protective role of anti-parkinsonian drugs in pancreatic cancer risk: A comprehensive case-control study in Taiwan.Cancer science · 2025Article
- Novel Insights into Psychosis and Antipsychotic Interventions: From Managing Symptoms to Improving Outcomes.International journal of molecular sciences · 2024Review
- The Role of Endocrine Disruption Chemical-Regulated Aryl Hydrocarbon Receptor Activity in the Pathogenesis of Pancreatic Diseases and Cancer.International journal of molecular sciences · 2024Review
- Tryptophan metabolism in digestive system tumors: unraveling the pathways and implications.Cell communication and signaling : CCS · 2024Review
- Amino acid transporter SLC38A5 is a tumor promoter and a novel therapeutic target for pancreatic cancer.Scientific reports · 2023Article
- Aryl Hydrocarbon Receptor as an Anticancer Target: An Overview of Ten Years Odyssey.Molecules (Basel, Switzerland) · 2023Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IDO1 is an immunomodulatory enzyme responsible for tryptophan catabolism. Its expression in immune cells, especially the DCs, has attracted attention because it leads to tryptophan depletion at the immunological synapse, thereby causing T-cell anergy and immune evasion by the tumor cells. Cancer cells also overexpress IDO1. Immunotherapy targeting IDO1 has been one of the focus areas in cancer biology, but lately studies have identified non-immune related functions of IDO1 leading to a paradigm shift with regard to IDO1 function in the context of tumor cells. In this study, we show that PDAC tissues and PDAC cells overexpress IDO1. The expression level is reciprocally related to overall patient survival. We further show that carbidopa, an FDA-approved drug for Parkinson's disease as well as an AhR agonist, inhibits IDO1 expression in PDAC cells. Using athymic nude mice, we demonstrate that carbidopa-mediated suppression of IDO1 expression attenuates tumor growth. Mechanistically, we show that AhR is responsible for carbidopa-mediated suppression of IDO1, directly as a transcription factor and indirectly by interfering with the JAK/STAT pathway. Overall, targeting IDO1 not only in immune cells but also in cancer cells could be a beneficial therapeutic strategy for PDAC and potentially for other cancers as well and that carbidopa could be repurposed to treat cancers that overexpress IDO1.
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