ArticleCell death & disease2017
MicroRNA-519a-3p mediates apoptosis resistance in breast cancer cells and their escape from recognition by natural killer cells.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.
- Tumor Immune Microenvironment and Its Related miRNAs in Tumor Progression.Frontiers in immunology · 2021Pooled it
- Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy.Pharmaceutical science advances · 2026Review
- Emerging role of microRNAs as modulators of the tumor immune microenvironment.Journal for immunotherapy of cancer · 2026Review
- Galangin's Therapeutic Potential in Retinoblastoma: Inducing Apoptosis and Modulating RB Protein and Some MicroRNAs.Advanced pharmaceutical bulletin · 2026Article
- NKGD2 Ligands (NKG2DLs) in Breast Cancer: In Silico Analysis and Narrative Review.International journal of molecular sciences · 2026Review
- Hypoxia Signaling and Non-Coding RNAs: Regulatory Networks and Therapeutic Implications in Breast Cancer.Current issues in molecular biology · 2026Review
- miR-99b-5p inhibition drives apoptosis and tumor shrinkage in triple-negative breast cancer: functional characterization through AGO2-RIP-seq and mechanistic insights.Frontiers in oncology · 2026Article
- MicroRNA-mediated regulation of natural killer cells development, effector functions, and antitumor responses.Cancer cell international · 2025Review
- Human miRNAs in Cancer: Statistical Trends and Cross Kingdom Approach.International journal of molecular sciences · 2025Article
- Expression Analysis of miR-519a-3p and miR-379-5p in Colorectal Cancer Patients: A Combined Experimental and Bioinformatic Approach.Diagnostics (Basel, Switzerland) · 2025Article
- MicroRNA-541-3p/Rac2 signaling bridges radiation-induced lung injury and repair.Non-coding RNA research · 2025Article
- Decoding breast cancer treatment resistance through genetic, epigenetic, and immune-regulatory mechanisms: from molecular insights to translational perspectives.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- Recent Insights Into Breast Cancer: Molecular Pathways, Epigenetic Regulation, and Emerging Targeted Therapies.Breast cancer : basic and clinical research · 2025Review
- Ambivalent roles of miRNAs in cancer development via modulating tumor-associated innate immune cells.BioImpacts : BI · 2025Review
- Natural killer cell-based cancer immunotherapy: from basics to clinical trials.Experimental hematology & oncology · 2024Review
- A potential mechanism of tumor immune escape: Regulation and application of soluble natural killer group 2 member D ligands (Review).Oncology reports · 2024Review
- Cell Death: Mechanisms and Potential Targets in Breast Cancer Therapy.International journal of molecular sciences · 2024Review
- Immune modulatory microRNAs in tumors, their clinical relevance in diagnosis and therapy.Journal for immunotherapy of cancer · 2024Review
- p53 at the crossroads of tumor immunity.Nature cancer · 2024Review
- miR-375-3p targets YWHAB to attenuate intestine injury in neonatal necrotizing enterocolitis.Pediatric surgery international · 2024Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aggressive breast cancer is associated with poor patient outcome and characterized by the development of tumor cell variants that are able to escape from control of the immune system or are resistant to targeted therapies. The complex molecular mechanisms leading to immune escape and therapy resistance are incompletely understood. We have previously shown that high miR-519a-3p levels are associated with poor survival in breast cancer. Here, we demonstrate that miR-519a-3p confers resistance to apoptosis induced by TRAIL, FasL and granzyme B/perforin by interfering with apoptosis signaling in breast cancer cells. MiR-519a-3p diminished the expression of its direct target genes for TRAIL-R2 (TNFRSF10B) and for caspase-8 (CASP8) and its indirect target gene for caspase-7 (CASP7), resulting in reduced sensitivity and tumor cell apoptosis in response to apoptotic stimuli. Furthermore, miR-519a-3p impaired tumor cell killing by natural killer (NK) cells via downregulation of the NKG2D ligands ULBP2 and MICA on the surface of tumor cells that are crucial for the recognition of these tumor cells by NK cells. We determined that miR-519a-3p was overexpressed in more aggressive mutant TP53 breast cancer that was associated with poor survival. Furthermore, low levels of TRAIL-R2, caspase-7 and caspase-8 correlated with poor survival, suggesting that the inhibitory effect of miR-519a-3p on TRAIL-R2 and caspases may have direct clinical relevance in lowering patient's prognosis. In conclusion, we demonstrate that miR-519a-3p is a critical factor in mediating resistance toward cancer cell apoptosis and impairing tumor cell recognition by NK cells. This joint regulation of apoptosis and immune cell recognition through miR-519a-3p supports the hypothesis that miRNAs are key regulators of cancer cell fate, facilitating cancer progression and evasion from immunosurveillance at multiple and interconnected levels.
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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.