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Updated: Apr 19, 2026
A Reporter Assay to Analyze Intronic microRNA Maturation in Mammalian Cells
Published on: June 16, 2022
Blocking the maturation of OncomiRNAs using pri-miRNA-17∼92 aptamer in retinoblastoma
Nithya Subramanian1, Jagat R Kanwar, Rupinder K Kanwar
11 Department of Nanobiotechnology, Vision Research Foundation, Kamalnayan Bajaj Institute for Research in Vision and Ophthalmology , Chennai, India .
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.
Insights
A novel pri-miRNA-17∼92 aptamer effectively targets retinoblastoma (RB) by inhibiting key oncogenic microRNAs. This aptamer demonstrated antiproliferative effects, inducing cell cycle arrest and apoptosis in RB cell lines.
Area of Science:
- Oncology
- Molecular Biology
- Biotechnology
Background:
- The miR-17∼92 cluster, also known as oncomiR-1, promotes retinoblastoma (RB) tumor formation.
- Current therapeutic strategies against oncogenic microRNAs (miRNAs) include antagomirs and miRNA mimics, with other methods still under development.
Purpose of the Study:
- To investigate the potential of a pri-miRNA-17∼92 aptamer (pri-apt) as a novel therapeutic agent against RB.
- To evaluate the efficacy of pri-apt in abrogating the maturation of specific oncogenic miRNAs (miR-17, miR-18a, miR-19b) involved in RB.
Main Methods:
- Utilized RB cell lines (WERI-Rb1 and Y79) as an in vitro model.
- Transfected cells with the pri-miRNA-17∼92 aptamer (pri-apt).
- Assessed cellular changes including cell cycle progression, apoptosis, cytotoxicity (lactate dehydrogenase activity), and cell proliferation.
Main Results:
- Pri-apt transfection led to S-phase arrest in WERI-Rb1 cells and induced apoptosis in both WERI-Rb1 and Y79 cell lines.
- Increased cytotoxicity was observed in pri-apt treated Y79 cells.
- Significant inhibition of cell proliferation was demonstrated in both RB cell lines.
Conclusions:
- The pri-miRNA-17∼92 aptamer exhibits significant antiproliferative properties against retinoblastoma cell lines.
- Pri-apt holds promise as a potential therapeutic strategy for RB, with possibilities for targeted delivery vector development.
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