ArticleAging cell2015
Mir-23a induces telomere dysfunction and cellular senescence by inhibiting TRF2 expression.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Telomeric autophagy in human health, aging, and diseases.Frontiers in molecular biosciences · 2026Review
- Senomorphic miR-3155b suppresses the senescence-associated secretory phenotype in therapy-induced senescence.Frontiers in cell and developmental biology · 2026Article
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- miR-23a-mediated TRF2 repression in CD4 T cells from PLWH.Molecular immunology · 2025Article
- Elucidation of how the Mir-23-27-24 cluster regulates development and aging.Experimental & molecular medicine · 2024Review
- Noncoding RNA Contribution to Aging and Lifespan.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Ginsenoside F1-Mediated Telomere Preservation Delays Cellular Senescence.International journal of molecular sciences · 2023Article
- EPAS1 prevents telomeric damage-induced senescence by enhancing transcription ofZoological research · 2023Article
- Neuronal Prosurvival Role of Ceramide Synthase 2 by Olidogendrocyte-to-Neuron Extracellular Vesicle Transfer.International journal of molecular sciences · 2023Article
- MiR-182-3p targets TRF2 and impairs tumor growth of triple-negative breast cancer.EMBO molecular medicine · 2023Article
- TRF2 inhibition rather than telomerase disruption drives CD4T cell dysfunction during chronic viral infection.Journal of cell science · 2022Article
- Telomere Targeting Approaches in Cancer: Beyond Length Maintenance.International journal of molecular sciences · 2022Review
- Identifying Common Genes and Pathways Associated with Periodontitis and Aging by Bioinformatics Analysis.Disease markers · 2022Article
- Review
- Prognostic value of TERF1 expression in prostate cancer.Journal of the Egyptian National Cancer Institute · 2021Article
- Abnormal function of telomere protein TRF2 induces cell mutation and the effects of environmental tumor‑promoting factors (Review).Oncology reports · 2021Review
- AhR/miR-23a-3p/PKCα axis contributes to memory deficits in ovariectomized and normal aging female mice.Molecular therapy. Nucleic acids · 2021Article
- miR-23a/b suppress cGAS-mediated innate and autoimmunity.Cellular & molecular immunology · 2021Article
- miR-490 suppresses telomere maintenance program and associated hallmarks in glioblastoma.Cellular and molecular life sciences : CMLS · 2021Article
- miR-376a Provokes Rectum AdenocarcinomaFrontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Telomeric repeat binding factor 2 (TRF2) is essential for telomere maintenance and has been implicated in DNA damage response and aging. Telomere dysfunction induced by TRF2 inhibition can accelerate cellular senescence in human fibroblasts. While previous work has demonstrated that a variety of factors can regulate TRF2 expression transcriptionally and post-translationally, whether microRNAs (miRNAs) also participate in post-transcriptionally modulating TRF2 levels remains largely unknown. To better understand the regulatory pathways that control TRF2, we carried out a large-scale luciferase reporter screen using a miRNA expression library and identified four miRNAs that could target human TRF2 and significantly reduce the level of endogenous TRF2 proteins. In particular, our data revealed that miR-23a could directly target the 3' untranslated region (3'UTR) of TRF2. Overexpression of miR-23a not only reduced telomere-bound TRF2 and increased telomere dysfunction-induced foci (TIFs), but also accelerated senescence of human fibroblast cells, which could be rescued by ectopically expressed TRF2. Our findings demonstrate that TRF2 is a specific target of miR-23a, and uncover a previously unknown role for miR-23a in telomere regulation and cellular senescence.
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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.