Toll-Like receptor 3-mediated interferon-β production is suppressed by oncostatin m and a broader epithelial-mesenchymal transition program
Our findings provide a novel insight into the regulation of TLR3 and IFN-β production in TNBC cells, which are known indicators of treatment responses to DNA-damaging therapies. Furthermore, strategies to stimulate TLR3 in order to increase IFN-β within the TME may be ineffective in stem-like/mesenchymal cells, as TLR3 is strongly repressed. Rather, we propose that therapies targeting OSM or OSM receptor would reverse the stem-like/mesenchymal program and restore TLR3-mediated IFN-β production within the TME, facilitating improved responses to current therapies.
Authors
- Kelsey L. Polak (ORCID: https://orcid.org/0000-0002-5127-3880)
- Ilaria Tamagno (ORCID: https://orcid.org/0000-0003-3572-8547)
- E. Ricky Chan (ORCID: https://orcid.org/0000-0001-9277-5329)
- Xueer Yuan (ORCID: https://orcid.org/0009-0001-5902-7895)
- Noah M. Chernosky (ORCID: https://orcid.org/0000-0001-6612-3538)
- Mark W. Jackson (ORCID: https://orcid.org/0000-0002-9249-5623)
Institutions
- University Hospitals Cleveland Medical Center (US)
- Case Comprehensive Cancer Center
- Case Western Reserve University (US)
Publication Details
- Journal
- Breast Cancer Research
- Published
- 2024-11-26
- DOI
- https://doi.org/10.1186/s13058-024-01918-2
- Citations
- 1
- Primary Topic
- Cytokine Signaling Pathways and Interactions
- Type
- article
- Field-Weighted Citation Impact
- 0.28
Funders
- National Institutes of Health