ArticleNucleic acid therapeutics2015
Blocking the maturation of OncomiRNAs using pri-miRNA-17∼92 aptamer in retinoblastoma.
Article in Nucleic acid therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Tumor heterogeneity in retinoblastoma: a literature review.Cancer metastasis reviews · 2025Review
- The Killer's Web: Interconnection between Inflammation, Epigenetics and Nutrition in Cancer.International journal of molecular sciences · 2024Review
- Retinoblastoma: A review of the molecular basis of tumor development and its clinical correlation in shaping future targeted treatment strategies.Indian journal of ophthalmology · 2023Review
- miRNAs in Cancer (Review of Literature).International journal of molecular sciences · 2022Review
- Expression profiles and prognostic value of miRNAs in retinoblastoma.Journal of cancer research and clinical oncology · 2019Review
- Non-Coding RNAs in Retinoblastoma.Frontiers in genetics · 2019Review
- Recent Advances in Nanoparticle-Based Cancer Drug and Gene Delivery.Advances in cancer research · 2018Review
- Identification of Autophagy-Related Genes and Their Regulatory miRNAs Associated with Celiac Disease in Children.International journal of molecular sciences · 2017Article
- Epigenetic regulation of human retinoblastoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Aptamers: A promising chemical antibody for cancer therapy.Oncotarget · 2016Review
- Small and Long Non-Coding RNAs: Novel Targets in Perspective Cancer Therapy.Current genomics · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The miR-17∼92. or oncomiR-1, cluster encodes oncogenic microRNAs (miRNAs), and it also promotes retinoblastoma (RB) tumor formation. Antagomir and miRNA mimics based approaches are widely tried against oncogenic and tumor suppressive miRNAs. Other methods for targeting cancer related miRNAs are still under development. In the current study, we focused on the pri-miRNA-17∼92 aptamer (pri-apt), which can potentially replace the mix of five antagomirs by one aptamer that function to abrogate the maturation of miR-17, miR-18a, and miR-19b (P<0.05) for targeting RB. We used RB cell lines WERI-Rb1 and Y79 as an in vitro model. Cellular changes upon transfecting the pri-apt led to S-phase arrest in WERI-Rb1 cells and onset of apoptosis in both Y79 and WERI-Rb1 cell lines. There was increased cytotoxicity as measured by lactate dehydrogenase activity in pri-apt treated Y79 cells (P<0.05), and significant inhibition of cell proliferation was observed in both of the cell lines. Thus we showed the antiproliferative property of pri-apt in RB cell lines, which can be readily modified by developing appropriate vectors for the delivery of the aptamer specifically to cancer cells.
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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.