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Published:
Feb 5, 2024DOI:
10.4314/tjpr.v23i1.2Keywords:
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Main Article Content
MiR-25 enhances the proliferation, invasion and migration of nasopharyngeal carcinoma cells through targeted regulation of RAGE expression
Abstract
Purpose: To determine the effect of microRNA-25 (miR-25) on the proliferation, invasion, and migration of nasopharyngeal carcinoma cells, and the involvement of targeted regulation of late glycation end product receptor (RAGE) in the process.
Methods: Three groups of cells comprising; routinely cultured nasopharyngeal normal epithelial cell line NP69 without any treatment (blank control group), untreated human nasopharyngeal carcinoma cell line 5-8F, also cultured routinely (nasopharyngeal carcinoma group) and 5-8F human nasopharyngeal carcinoma cells infected with lentiviral vectors for miR-25 gene knockdown and cultured after stable transduction (miR-25 knockdown group). Cell proliferation was assessed using CCK-8 assay, while Western blot assay and quantitative polymerase chain reaction (qPCR) were used to measure protein and mRNA expression levels of relevant genes. Transwell assay was utilized to evaluate cell migration and invasion.
Results: The miR-25 expression level was significantly increased in nasopharyngeal carcinoma group (p < 0.05). Cell proliferation, migration, and invasion rates in miR-25 knockdown group were lower than those in nasopharyngeal carcinoma group (p < 0.05). Apoptosis rate of cells and levels of apoptotic proteins were significantly elevated, whereas bcl-2 level was significantly reduced in miR-25 knockdown group when compared to nasopharyngeal carcinoma group (p < 0.05). Protein expression levels of RAGE and S100P was significantly increased in nasopharyngeal carcinoma group, but significantly down-regulated in miR-25 knockdown group (p < 0.05). Conclusion: Expression of miR-25 increases in nasopharyngeal carcinoma cells. Suppression of miR25 results in decreased viability of nasopharyngeal carcinoma cells and inhibits cell proliferation, migration, and invasion, while enhancing apoptosis. The mechanism underlying these effects was associated with modulation of protein expressions of RAGE and S100P. Targeted regulation of late glycation end-product receptors hold promising potential as prospective biomarker for therapeutic interventions targeting specific cancers.
