The Effect of miR-32-5p Targeting ITGAV on the Proliferation, Invasion, Migration and Apoptosis of OS Cells
- 1 School of Clinical Medicine, Youjiang Medical University for Nationalities, Baise, China
- 2 School of Clinical Medicine, Youjiang Medical University for Nationalities, Baise, China
- 3 School of Clinical Medicine, Youjiang Medical University for Nationalities, Baise, China
- 4 School of Clinical Medicine, Youjiang Medical University for Nationalities, Baise, China
- 5 School of Clinical Medicine, Youjiang Medical University for Nationalities, Baise, China
- 6 School of Clinical Medicine, Youjiang Medical University for Nationalities, Baise, China
- 7 The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China
Abstract
Objective: This study aims to analyze the regulatory mechanism of miR-32-5p on the biological behavior of osteosarcoma (OS) cells and to elucidate the role and mechanism of miR-32-5p in OS. Methods: TargetScan, dual-luciferase reporter gene assays, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and Western blotting were employed to confirm whether ITGAV serves as the target gene of miR-32-5p. qRT-PCR was utilized to assess the impact of up-regulated miR-32-5p on ITGAV mRNA levels. Cell proliferation, invasion, and migration were evaluated using the CCK-8 assay and Transwell chamber, while the effects of miR-32-5p and ITGAV on the apoptosis of MG63 cells were analyzed through flow cytometry. Results: Experimental findings demonstrated that miR-32-5p specifically binds to the 3'-UTR of ITGAV, thereby regulating its expression. The miR-32-5p mimics group significantly inhibited the expression levels of both ITGAV mRNA and its protein. Concurrently, the expression of the pro-apoptotic protein BAX increased, while the levels of the anti-apoptotic protein BCL2 decreased. Furthermore, the miR-32-5p mimics group inhibited the proliferation, invasion, and migration capabilities of MG63 OS cells and promoted their apoptosis. Conclusion: miR-32-5p exerts an inhibitory effect on the proliferation, invasion, and migration of OS cells while promoting their apoptosis by targeting and down-regulating ITGAV expression, indicating its potential as a therapeutic agent in OS.
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