ArticleMolecular cancer2026
piR-1170 drives brain metastasis and immune evasion via WTAP-mediated m6A methylation reprogramming in triple-negative breast cancer.
Article in Molecular cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- An evidence informed framework for artificial intelligence in rare breast cancers using small cohort validation synthetic data practices and clinical governance.Discover oncology · 2026Review
- GPR17 Suppresses Triple-Negative Breast Cancer Progression and Serves as an Independent Prognostic Biomarke.World journal of surgical oncology · 2026Article
- Novel Perspective for Prognostic Stratification and Personalized Therapy in Breast Cancer Patients: Development of Cancer Stem Cells and Metabolism-Associated Prognostic Model.International journal of women's health · 2026Article
- PARK2-Mediated PGK1 Degradation Suppresses Partial Epithelial-Mesenchymal Transition and Metastasis in Triple-Negative Breast Cancer.Oncology research · 2026Article
- RNA epitranscriptomic regulation of tumor immune evasion: mechanisms, context-dependent roles, and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Therapeutic target for triple-negative breast cancer (TNBC) brain metastases remains a critical unmet clinical challenge. The roles of PIWI-interacting RNAs (piRNAs) in driving brain metastasis are poorly understood, despite their known dysregulation and oncogenic functions in cancer. Here, we identified piR-1170 as a clinically relevant driver of TNBC brain metastasis through multi-model validation. Analysis of the TNBC cohort from Sun Yat-sen University Cancer Center revealed significant piR-1170 upregulation in brain metastases correlating with poor patient survival. First, upstream analysis confirmed that hnRNPK binds to piR-1170 to maintain the piRNA's stability, thereby sustaining piR-1170 upregulation in TNBC. Then, Functional studies with metastasis models demonstrated the brain-specific metastatic activity of piR-1170, enhancing tumor cell adhesion to brain endothelia, vascular extravasation, and parenchymal invasion. Mechanistically, piR-1170 promotes WTAP expression to enhance m6A methylation of DGAT2 and CD274 transcripts, activating de novo lipid synthesis and PD-L1-driven immune suppression to promote tumor adaptation to lipid-scarce metastases and avoid immune surveillance. Our study defined the piR-1170-driven axis that operates through coordinated metabolic reprogramming and immunosuppression, thus revealing its potential as a therapeutic candidate for TNBC brain metastasis.
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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.