ArticleScientific reports2024
Aryl hydrocarbon receptor suppresses STING-mediated type I IFN expression in triple-negative breast cancer.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 9 citations in OpenAlex.
- Biomarker identification of triple negative breast cancer subtypes using machine learning.NPJ systems biology and applications · 2026Article
- Two orthobunyaviruses: OYAV and EBIV co-opt the AhR-CYP1A1 axis to suppress type I interferon responses.Virologica Sinica · 2026Article
- IK-175, an Oral Aryl Hydrocarbon Receptor Inhibitor, Alone and with Nivolumab in Patients with Advanced Solid Tumors and Urothelial Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- PARP7 and aryl hydrocarbon receptor differentially regulate mammary cancer cell proliferation and STING-induced type I interferon signalling.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Aryl hydrocarbon receptor restrains tonic cytokine responses by inhibiting microbiota sensing in monocytes.The Journal of clinical investigation · 2025Article
- AhR deficiency exacerbates inflammation in diabetic wounds via impaired mitophagy and cGAS-STING-NLRP3 activation: Therapeutic potential of hydrogels loaded with FICZ.Materials today. Bio · 2025Article
- Therapeutic resistance and combination therapy for cancer: recent developments and future directions.Scientific reports · 2025Article
- Interplay between AHR genotypes, lifestyle factors and adjuvant breast cancer treatments significantly impacts clinical outcome in a population-based cohort.BJC reports · 2025Article
- Inosine monophosphate dehydrogenase 2 (IMPDH2) modulates response to therapy and chemo-resistance in triple negative breast cancer.Scientific reports · 2025Article
- The aryl hydrocarbon receptor as a tumor modulator: mechanisms to therapy.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is one of the most aggressive types of cancer. Despite decades of intense investigation, treatment options remain limited, and rapid recurrence with distant metastases remains a significant challenge. Cancer cell-intrinsic production of cytokines such as type I interferons (IFN-I) is a known potent modulator of response to therapy in many cancers, including TNBC, and can influence therapeutic outcome. Here, we report that, in TNBC systems, the aryl hydrocarbon receptor (AhR) suppresses IFN-I expression via inhibition of STImulator of Interferon Genes (STING), a key mediator of interferon production. Intratumoral STING activity is essential in mediating the efficacy of PARP inhibitors (PARPi) which are used in the treatment of cancers harboring BRCA1 deficiency. We find that, in TNBC cells, PARPi treatment activates AhR in a BRCA1 deficiency-dependent manner, thus suggesting the presence of a negative feedback loop aimed at modulating PARPi efficacy. Importantly, our results indicate that the combined inhibition of PARP and AhR is superior in elevating IFN-I expression as compared to PARPi-alone. Thus, AhR inhibition may allow for enhanced IFN-I production upon PARPi in BRCA1-deficient breast cancers, most of which are of TNBC origin, and may represent a therapeutically viable strategy to enhance PARPi efficacy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.