ArticleJournal of immunology (Baltimore, Md. : 1950)2019
Progesterone Receptor Attenuates STAT1-Mediated IFN Signaling in Breast Cancer.
Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- A Systematic Review of Lymphangioleiomyomatosis on Diagnosis and Molecular Mechanism.BioMed research international · 2021Pooled it
- IGFBP-6 regulates SH2D4A expression to promote breast cancer cell cycle progression in response to progesterone.Frontiers in endocrinology · 2026Article
- Multiplexed Imaging Mass Cytometry Reveals Tumor-immune Microenvironment-dependent Hormone Receptor Expression in Adult-Type Ovarian Granulosa Cell Tumors.Cancer research communications · 2025Article
- Progesterone receptor-dependent downregulation of MHC class I promotes tumor immune evasion and growth in breast cancer.Journal for immunotherapy of cancer · 2025Article
- High tumor glucocorticoid receptor expression in early-stage, triple-negative breast cancer is associated with increased T-regulatory cell infiltration.Breast cancer research and treatment · 2025Article
- Igniting Cold Tumors: Multi-Omics-Driven Strategies to Overcome Immune Evasion and Restore Immune Surveillance.Oncology research · 2025Review
- Vaccines targetingHuman vaccines & immunotherapeutics · 2024Article
- mScientific reports · 2024Article
- Site-specific O-GlcNAcylation of progesterone receptor (PR) supports PR attenuation of interferon stimulated genes (ISGs) and tumor growth in breast cancer.The Journal of biological chemistry · 2024Article
- Neurons upregulate PD-L1 via IFN/STAT1/IRF1 to alleviate damage by CD8Journal of neuroinflammation · 2024Article
- Estrogen Receptor Alpha Mutations, Truncations, Heterodimers, and Therapies.Endocrinology · 2024Review
- Estrogen receptor α-mediated signaling inhibits type I interferon response to promote breast carcinogenesis.Journal of molecular cell biology · 2024Article
- Comparative- and network-based proteomic analysis of bacterial chondronecrosis with osteomyelitis lesions in broiler's proximal tibiae identifies new molecular signatures of lameness.Scientific reports · 2023Article
- The Great Immune Escape: Understanding the Divergent Immune Response in Breast Cancer Subtypes.Cancer discovery · 2023Review
- The recent progress of endocrine therapy-induced osteoporosis in estrogen-positive breast cancer therapy.Frontiers in oncology · 2023Review
- Tailoring therapies to counter the divergent immune landscapes of breast cancer.Frontiers in cell and developmental biology · 2023Review
- STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Seminars in cancer biology · 2022Review
- Direct and indirect effects of IFN-α2b in malignancy treatment: not only an archer but also an arrow.Biomarker research · 2022Review
- Causal Discovery in High-dimensional, Multicollinear Datasets.Frontiers in epidemiology · 2022Article
- The Role of Progesterone Receptors in Breast Cancer.Drug design, development and therapy · 2022Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
Why some tumors remain indolent and others progress to clinical relevance remains a major unanswered question in cancer biology. IFN signaling in nascent tumors, mediated by STAT1, is a critical step through which the surveilling immune system can recognize and destroy developing tumors. In this study, we have identified an interaction between the progesterone receptor (PR) and STAT1 in breast cancer cells. This interaction inhibited efficient IFN-induced STAT1 phosphorylation, as we observed a decrease in phospho-STAT1 in response to IFN treatment in PR-positive breast cancer cell lines. This phenotype was further potentiated in the presence of PR ligand. In human breast cancer samples, PR-positive tumors exhibited lower levels of phospho-STAT1 as compared with their PR-negative counterparts, indicating that this phenotype translates to human tumors. Breast cancer cells lacking PR exhibited higher levels of IFN-stimulated gene (ISG) RNA, the transcriptional end point of IFN activation, indicating that unliganded PR alone could decrease transcription of ISGs. Moreover, the absence of PR led to increased recruitment of STAT1, STAT2, and IRF9 (key transcription factors necessary for ISG transcription) to ISG promoters. These data indicate that PR, both in the presence and absence of ligand, attenuates IFN-induced STAT1 signaling, culminating in significantly abrogated activation of genes transcribed in response to IFNs. PR-positive tumors may use downregulation of STAT1-mediated IFN signaling to escape immune surveillance, leading to the development of clinically relevant tumors. Selective immune evasion of PR-positive tumors may be one explanation as to why over 65% of breast cancers are PR positive at the time of diagnosis.
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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 OpenQuestion graph.