ArticleGenes & development2011
miR-17~92 cooperates with RB pathway mutations to promote retinoblastoma.
Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- Highly ordered architecture of microRNA cluster.BioMed research international · 2013Pooled it
- Global research landscape of retinoblastoma biomarkers: a multidisciplinary bibliometric analysis based on multiple databases (2005-2025).Journal of cancer research and clinical oncology · 2025Article
- Insights into retinoblastoma pathogenesis: unraveling RB1, N-MYC and miRNA profiles.BMJ open ophthalmology · 2025Article
- Tumor heterogeneity in retinoblastoma: a literature review.Cancer metastasis reviews · 2025Review
- Histopathology and molecular pathology of pediatric pineal parenchymal tumors.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2023Review
- Epigenetic Alterations in Canine Malignant Lymphoma: Future and Clinical Outcomes.Animals : an open access journal from MDPI · 2023Review
- Article
- Overexpression of miR-17 predicts adverse prognosis and disease recurrence for acute myeloid leukemia.International journal of clinical oncology · 2022Article
- Retinoblastoma: Review and new insights.Frontiers in oncology · 2022Review
- microRNA-based diagnostic and therapeutic applications in cancer medicine.Wiley interdisciplinary reviews. RNA · 2021Review
- Systematically Studying the Effect of Small Molecules Interacting with RNA in Cellular and Preclinical Models.ACS chemical biology · 2021Review
- Retinoblastoma cell-derived exosomes promote angiogenesis of human vesicle endothelial cells through microRNA-92a-3p.Cell death & disease · 2021Article
- Retinoblastoma tumor cell proliferation is negatively associated with an immune gene expression signature and increased immune cells.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Role of MicroRNAs in Human Osteosarcoma: Future Perspectives.Biomedicines · 2021Review
- microRNAs as Novel Therapeutics in Cancer.Cancers · 2021Review
- Small molecule recognition of disease-relevant RNA structures.Chemical Society reviews · 2020Review
- Review
- MicroRNA-19a-PTEN Axis Is Involved in the Developmental Decline of Axon Regenerative Capacity in Retinal Ganglion Cells.Molecular therapy. Nucleic acids · 2020Article
- Targeted Degradation of the Oncogenic MicroRNA 17-92 Cluster by Structure-Targeting Ligands.Journal of the American Chemical Society · 2020Article
- Pineoblastoma segregates into molecular sub-groups with distinct clinico-pathologic features: a Rare Brain Tumor Consortium registry study.Acta neuropathologica · 2020Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
The miR-17~92 cluster is a potent microRNA-encoding oncogene. Here, we show that miR-17~92 synergizes with loss of Rb family members to promote retinoblastoma. We observed miR-17~92 genomic amplifications in murine retinoblastoma and high expression of miR-17~92 in human retinoblastoma. While miR-17~92 was dispensable for mouse retinal development, miR-17~92 overexpression, together with deletion of Rb and p107, led to rapid emergence of retinoblastoma with frequent metastasis to the brain. miR-17~92 oncogenic function in retinoblastoma was not mediated by a miR-19/PTEN axis toward apoptosis suppression, as found in lymphoma/leukemia models. Instead, miR-17~92 increased the proliferative capacity of Rb/p107-deficient retinal cells. We found that deletion of Rb family members led to compensatory up-regulation of the cyclin-dependent kinase inhibitor p21Cip1. miR-17~92 overexpression counteracted p21Cip1 up-regulation, promoted proliferation, and drove retinoblastoma formation. These results demonstrate that the oncogenic determinants of miR-17~92 are context-specific and provide new insights into miR-17~92 function as an RB-collaborating gene in cancer.
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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.