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Updated: Jan 30, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Rn7SK small nuclear RNA is involved in cellular senescence
Maryam Musavi1,2, Fatemeh Kohram3, Mozhgan Abasi2,4
1Department of Biotechnology, School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Rn7SK is a conserved small nuclear noncoding RNA which its function in aging has not been studied. Recently, we have demonstrated that Rn7SK overexpression reduces cell viability and is significantly downregulated in stem cells, human tumor tissues, and cell lines. In this study, we analyzed the role of Rn7SK on senescence in adipose tissue-derived mesenchymal stem cells (AD-MSCs). For this purpose, Rn7SK expression was downregulated and upregulated via transfection and transduction, respectively, in AD-MSCs and subsequently, various distinct characteristics of senescence including cell viability, proliferation, colony formation, senescence-associated β galactosidase activity, and differentiation potency was analyzed. Our results demonstrated the transient knockdown of Rn7SK in MSCs leads to delayed senescence, while its overexpressions shows opposite effects. When osteogenic differentiation was started, however, they exhibited a greater differentiation potential than the original MSCs, suggesting a potential tool for stem cell-based regenerative medicine.
Insights
The small nuclear noncoding RNA Rn7SK influences cell aging. Its downregulation delays senescence in mesenchymal stem cells, while overexpression accelerates it, offering potential for regenerative medicine.
Area of Science:
- Molecular Biology
- Cell Biology
- Aging Research
Background:
- The function of the conserved small nuclear noncoding RNA Rn7SK in aging remains largely uncharacterized.
- Previous studies indicated Rn7SK overexpression reduces cell viability and is downregulated in various cancer and stem cell contexts.
Purpose of the Study:
- To investigate the role of Rn7SK in cellular senescence.
- To analyze the impact of Rn7SK modulation on adipose tissue-derived mesenchymal stem cells (AD-MSCs).
Main Methods:
- Manipulated Rn7SK expression in AD-MSCs using transfection (downregulation) and transduction (upregulation).
- Assessed senescence hallmarks: cell viability, proliferation, colony formation, and senescence-associated β-galactosidase activity.
- Evaluated the effect on osteogenic differentiation potential.
Main Results:
- Transient knockdown of Rn7SK expression in AD-MSCs resulted in delayed senescence.
- Overexpression of Rn7SK led to accelerated senescence.
- AD-MSCs with altered Rn7SK expression showed enhanced osteogenic differentiation potential.
Conclusions:
- Rn7SK plays a significant role in regulating cellular senescence in AD-MSCs.
- Modulating Rn7SK offers a potential strategy for enhancing stem cell differentiation for regenerative medicine applications.
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