ArticleImmunologic research2024
The combination of IDO and AHR blockers reduces the migration and clonogenicity of breast cancer cells.
Article in Immunologic research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Network toxicology and multiomics reveal bisphenol A-mediated immune evasion in breast cancer.The Journal of international medical research · 2025Article
- Naringenin Exhibits Antiglioma Activity Related to Aryl Hydrocarbon Receptor Activity and IL-6, CCL2, and TNF-α Expression.Brain sciences · 2025Article
- The combination of IDO and AHR blockers reduces the migration and clonogenicity of breast cancer cells.Immunologic research · 2024Article
- Landscape of unconventional γδ T cell subsets in cancer.Molecular biology reports · 2024Review
- Landscape of unconventional γδ T cell subsets in cancer.Molecular biology reports · 2024Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The indoleamine-2,3-dioxygenase (IDO) enzyme causes immunosuppressive consequences in the tumor microenvironment (TME). In addition, the role of aryl hydrocarbon receptor (AHR) in the TME is under discussion. The current study evaluated the role of the IDO and AHR blockers on cell migration, clonogenic, and IDO expression of murine breast cancer cells. The cell migration and clonogenic abilities of breast cancer cells are evaluated by wound‑healing assay (cell migration assay) and Colony formation assay (clonogenic assay). Also, flow cytometry analysis was used to detect the IDO-positive breast cancer cells. The results showed that treating cells with a combination of IDO and AHR blockers dramatically reduced breast cancer cells' migration and clonogenic capacities. Treating cells with only AHR blockade suppressed the clonogenic rate. Since both IDO and AHR are involved in their complex molecular networks, blocking both IDO and AHR might cause alterations in their molecular networks resulting in diminishing the migration and clonogenic abilities of breast cancer cells. However, further investigations are required to confirm our findings within in vivo models as a novel therapy for breast cancer.
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Registered trials
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