Abstract:Objective: To study the effect of IRF1 gene on proliferation and apoptosis of tongue squamous carcinoma cells and its upstream regulation mechanism by miR-23a. Methods: The expression level of IRF1 gene was detected by Real-time PCR in tongue squamous carcinoma tissues. The overexpression plasmid of IRF1 was constructed, and the effects of IRF1 on proliferation and apoptosis of tongue squamous carcinoma cells were examined by MTT assay and TUNEL assay, respectively. Bioinformatic predictions as well as fluorescent reporter vector assays verified that IRF1 was a direct target gene for miR-23a. The expression level of miR-23a in tongue squamous carcinoma tissues and the alteration of proliferation and apoptosis of tongue squamous carcinoma cells after the expression of miR-23a was further examined.Results: IRF1 expression levels were significantly lower in tongue squamous carcinoma tissues compared to paraneoplastic normal tissues. Overexpression of IRF1 in tongue squamous carcinoma cells resulted in a significant decrease in cell growth activity and an increase in paclitaxel-induced apoptosis index. TargetScan predicted that miR-23a could bind to the 3 'UTR of IRF1. It was confirmed that miR-23a could directly bind to the 3'UTR of IRF1 and thus regulate the expression of IRF1. The expression of miR-23a was abnormally elevated in tongue squamous carcinoma tissues, and after the expression of miR-23a was blocked, the growth activity of tongue squamous carcinoma cells was significantly decreased, while the apoptosis index induced by paclitaxel was increased, which was consistent with the results obtained from overexpression of IRF1. Conclusion: IRF1 is regulated by miR-23a to inhibit the growth activity and promote apoptosis of tongue squamous carcinoma cells. IRF1 is a tumor suppressor gene in the occurrence and development of tongue squamous cell carcinoma, while miR-23a, as an upstream regulator of IRF1, is also an oncogene of tongue squamous cell carcinoma.
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