ArticleCell communication and signaling : CCS2023
Opposite and dynamic regulation of the interferon response in metastatic and non-metastatic breast cancer.
Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 18 citations in OpenAlex.
- Reduction of primary tumor growth and metastasis in models of triple-negative breast cancer following tilorone administration via type I interferon signaling.Breast cancer research : BCR · 2026Article
- Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026Review
- Prunella vulgaris seed oil alleviates cancer related fatigue through hypothalamic inflammation and CRH regulation.NPJ science of food · 2025Article
- Collisional Cross-Section Prediction for Multiconformational Peptide Ions with IM2Deep.Analytical chemistry · 2025Article
- Spatial gene expression profiling identifies prognostic features of residual tumors after neoadjuvant chemotherapy in triple-negative breast cancer.Frontiers in oncology · 2025Article
- Toll-Like receptor 3-mediated interferon-β production is suppressed by oncostatin m and a broader epithelial-mesenchymal transition program.Breast cancer research : BCR · 2024Article
- Elucidating the power of arginine restriction: taming type I interferon response in breast cancer via selective autophagy.Cell communication and signaling : CCS · 2024Article
- Identification of modules and key genes associated with breast cancer subtypes through network analysis.Scientific reports · 2024Article
- NUPR1 packaged in extracellular vesicles promotes murine triple-negative breast cancer in a type 1 interferon-independent manner.Extracellular vesicles and circulating nucleic acids · 2024Article
- Review
- SARS-CoV-2 infection as a potential risk factor for the development of cancer.Frontiers in molecular biosciences · 2023Review
- Interferon-tau (IFN-τ) Has Antiproliferative Effects, Induces Apoptosis, and Inhibits Tumor Growth in a Triple-negative Breast Cancer Murine Tumor Model.In vivo (Athens, Greece)Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo our current understanding, solid tumors depend on suppressed local immune reactions, often elicited by the interaction between tumor cells and tumor microenvironment (TME) components. Despite an improved understanding of anti-cancer immune responses in the TME, it is still unclear how immuno-suppressive TME are formed and how some cancer cells survive and metastasize.
methodsTo identify the major adaptations that cancer cells undergo during tumor development and progression, we compared the transcriptome and proteome from metastatic 66cl4 and non-metastatic 67NR cell lines in culture versus their corresponding mouse mammary primary tumors. Using confocal microscopy, RT-qPCR, flow cytometry and western blotting, we studied the signaling pathway and the mechanisms involved. In addition, we used public gene expression data from human breast cancer biopsies to evaluate the correlation between gene expression and clinical outcomes in patients.
resultsWe found that type I interferon (IFN-I) response was a key differentially regulated pathway between metastatic and non-metastatic cell lines and tumors. The IFN-I response was active in metastatic cancer cells in culture and markedly dampened when these cells formed primary tumors. Interestingly, the opposite was observed in non-metastatic cancer cells and tumors. Consistent with an active IFN-I response in culture, the metastatic cancer cells displayed elevated levels of cytosolic DNA from both mitochondria and ruptured micronuclei with concomitant activation of cGAS-STING signaling. Interestingly, decreased IFN-I-related gene expression in breast cancer biopsies correlated with an unfavourable prognosis in patients.
conclusionOur findings show that IFN-I response is dampened in the tumors with the metastatic ability and lower IFN-I expression predicts poor prognosis in triple-negative and HER2 enriched breast cancer patients. This study highlights the possibility of reactivating the IFN-I response as a potential therapeutic strategy in breast cancer. Video Abstract.
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