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MicroRNA-31 promotes chondrocyte proliferation by targeting C-X-C motif chemokine ligand 12
The present study aimed to investigate the biological function and underlying molecular mechanisms of miR-31 in osteoarthritis (OA). Reverse transcription-quantitative polymerase chain reaction was used to detect miR-31 expression, and it was found that miR-31 was downregulated in the cartilage tiss...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390014/ https://www.ncbi.nlm.nih.gov/pubmed/30664157 http://dx.doi.org/10.3892/mmr.2019.9859 |
Sumario: | The present study aimed to investigate the biological function and underlying molecular mechanisms of miR-31 in osteoarthritis (OA). Reverse transcription-quantitative polymerase chain reaction was used to detect miR-31 expression, and it was found that miR-31 was downregulated in the cartilage tissues of OA patients. microRNA.org was used to predict the gene targets of miR-31, and dual luciferase reporter assays were used to verify that C-X-C motif chemokine ligand 12 (CXCL12) was a direct target of miR-31. The human chondrocyte cell line CHON-001 was used to perform MTT and cell migration assays. Western blotting was used to measure the protein expression of CXCL12, type I collagen and aggrecan. The results suggested that CXCL12 was a target of miR-31, and the expression of CXCL12 was negatively regulated by miR-31 in CHON-001 cells. miR-31 increased CHON-001 cell viability and migration, as well as the expression of type I collagen and aggrecan. Furthermore, the overexpression of CXCL12 eliminated the effects of miR-31 mimics on CHON-001 cells. In conclusion, the data indicated that miR-31 promoted chondrocyte viability and migration by directly targeting CXCL12, which provided evidence for CXCL12 as a potential target in OA therapy. |
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