关键词: 鼻咽癌, PRNCR1, miR-653-5p, 细胞增殖, 凋亡, 迁移, 侵袭

Abstract: Objective To investigate the effect of long non-coding RNA(lncRNA) PRNCR1 on the malignant biological behavior of nasopharyngeal carcinoma cells and its possible mechanism. Methods The expressions of PRNCR1 and miR-653-5p in the Nasopharyngeal carcinoma cell lines(5-8F, 6-10B, C666-1) and nasopharyngeal epithelial cells NP69 were detected by RT-qPCR.  The si-PRNCR1 and miR-653-5p mimics or co-transfected with si-PRNCR1 and anti-miR-653-5p, were transfected into nasopharyngeal carcinoma 6-10B cells，respectively. The cell proliferation was detected by CCK-8 method, cell apoptosis was detected by flow cytometry, cell migration was detected by scratch test, cell invasion was detected by Transwell chamber test, and the targeting relationship between PRNCR1 and miR-653-5p was verified by the dual luciferase reporter gene experiment. Results The expression level of PRNCR1 in nasopharyngeal carcinoma cell lines (5-8F, 6-10B, C666-1) was higher than that of nasopharyngeal epithelial cells NP69 (all P<0.001), while the expression level of miR-653-5p was lower than that of NP69 cells(all P<0.001). After knocking down PRNCR1 or overexpressing miR-653-5p, the proliferation ability, scratch healing rate and invasion number of nasopharyngeal carcinoma 6-10B cells were decreased (all P<0.001), but the apoptosis rate was increased (all P<0.001). The dual luciferase reporter assay confirmed that PRNCR1 had a targeting relationship with miR-653-5p. After knocking down PRNCR1, the expression level of miR-653-5p in 6-10B cells was increased (P<0.001). Knocking down miR-653-5p could reverse the effect of knocking down PRNCR1 on the proliferation, apoptosis, migration and invasion of nasopharyngeal carcinoma 6-10B cells. Conclusions PRNCR1 is highly expressed in nasopharyngeal carcinoma cell lines. The knockdown of PRNCR1 expression can inhibit the proliferation, migration and invasion of nasopharyngeal carcinoma cells, and promote cells apoptosis. The underlying mechanism may be related to the targeted negative regulation of miR-653-5p.

Key words:  Nasopharyngeal carcinoma, PRNCR1, miR-653-5p, Cell proliferation, Apoptosis, Migration, Invasion