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Updated: Dec 31, 2025
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
MiR93-5p inhibits chondrocyte apoptosis in osteoarthritis by targeting lncRNA CASC2
Yun Sun1, Simiao Kang2, Shuyan Pei1
1Department of Orthopaedics, Jiujiang University Clinical Medical College·Jiujiang University Hospital, No.57 Xunyang East Road, Jiujiang City, jiangxi Province, 332000, People's Republic of China.
Background:
It has been reported that miR-93-5p and long non-coding RNA (lncRNA) Cancer Susceptibility 2 (CASC2) play opposite roles in regulating chondrocyte apoptosis, indicating the possible interaction between them. This study aimed to investigate the interaction between miR-93-5p and lncRNA CASC2 in chondrocyte apoptosis, which plays critical roles in osteoarthritis (OA).
Methods:
The interaction between CASC2 and miR-93-5p was analyzed by dual luciferase assay and overexpression experiments. Levels of CASC2 and miR-93-5p in plasma sample from OA patients and healthy controls were measured by RT-qPCR. The roles of CASC2 and miR-93-5p in regulating the apoptosis of chondrocyte induced by LPS were analyzed by cell apoptosis assay.
Results:
Through bioinformatics analysis we observed the potential interaction between CASC2 and miR-93-5p, which was confirmed by dual luciferase assay. In OA patients, miR-93-5p was downregulated, while CASC2 was upregulated, and they were inversely correlated. LPS treatment led to downregulated miR-93-5p and upregulated CASC2. Overexpression of miR-93-5p led to the downregulated CASC2 in chondrocytes. Under LPS treatment, CASC2 overexpression promoted the apoptosis of chondrocyte. MiR-93-5p overexpression played an opposite role and attenuated the effects of CASC2 overexpression.
Conclusion:
MiR-93-5p was downregulated in OA may inhibit LPS-induced chondrocyte apoptosis by targeting lncRNA CASC2.
Insights
MicroRNA-93-5p (miR-93-5p) is downregulated in osteoarthritis (OA) and may inhibit chondrocyte apoptosis by targeting long non-coding RNA CASC2. This interaction is crucial for understanding OA pathogenesis.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Chondrocyte apoptosis is critical in osteoarthritis (OA) pathogenesis.
- MicroRNA-93-5p (miR-93-5p) and long non-coding RNA Cancer Susceptibility 2 (CASC2) exhibit opposing roles in chondrocyte apoptosis.
- A potential interaction between miR-93-5p and CASC2 warrants investigation in OA.
Purpose of the Study:
- To investigate the interaction between miR-93-5p and CASC2 in the context of chondrocyte apoptosis.
- To determine the expression levels of miR-93-5p and CASC2 in osteoarthritis patients.
- To elucidate the regulatory roles of miR-93-5p and CASC2 in lipopolysaccharide (LPS)-induced chondrocyte apoptosis.
Main Methods:
- Bioinformatics analysis, dual luciferase assay, and overexpression experiments were used to confirm the interaction between CASC2 and miR-93-5p.
- Quantitative real-time PCR (RT-qPCR) was employed to measure CASC2 and miR-93-5p levels in plasma from OA patients and healthy controls.
- Cell apoptosis assays were performed to analyze the roles of CASC2 and miR-93-5p in LPS-induced chondrocyte apoptosis.
Main Results:
- Bioinformatics and dual luciferase assays confirmed the interaction between CASC2 and miR-93-5p.
- Osteoarthritis patients showed downregulated miR-93-5p and upregulated CASC2, with an inverse correlation.
- LPS treatment decreased miR-93-5p and increased CASC2; CASC2 overexpression promoted chondrocyte apoptosis, while miR-93-5p overexpression attenuated this effect.
Conclusions:
- MiR-93-5p is downregulated in osteoarthritis.
- Downregulated miR-93-5p may promote LPS-induced chondrocyte apoptosis by targeting CASC2.
- The miR-93-5p/CASC2 axis is a potential therapeutic target for osteoarthritis.
