LncRNA PRNCR1靶向miR-653-5p调控鼻咽癌细胞恶性生物学行为  

Regulation of the malignant biological behavior of nasopharyngeal carcinoma cells by lncRNA PRNCR1 targeting miR-653-5p

作　　者：赵黎阳[1] 崔玲[1] 张颖[1] 王玲[1] 李会政[1] ZHAO Liyang;CUI Ling;ZHANG Ying;WANG Ling;LI Huizheng(Department of Otolaryngology Head and Neck Surgery,Dalian Friendship Hospital,Dalian 116001,China)

机构地区：[1]大连市友谊医院耳鼻咽喉头颈外科,大连116001

出　　处：《中国癌症防治杂志》2021年第4期400-406,共7页CHINESE JOURNAL OF ONCOLOGY PREVENTION AND TREATMENT

基　　金：大连市科技计划项目(2019E15SF160)。

摘　　要：目的探讨前列腺癌非编码RNA 1(prostate cancer non-coding RNA 1,PRNCRl)对鼻咽癌细胞恶性生物学行为的影响及其可能的机制。方法采用RT-qPCR法检测鼻咽癌细胞系(5-8F、6-10B、C666-1)及鼻咽上皮细胞NP69中PRNCR1和miR-653-5p表达。分别将si-PRNCR1、miR-653-5p mimics或两者共转染至鼻咽癌6-10B细胞,采用CCK-8法检测细胞的增殖能力,流式细胞术检测细胞的凋亡情况,划痕实验检测细胞的迁移能力,Transwell小室实验检测细胞的侵袭能力,双荧光素酶报告基因实验验证PRNCR1和miR-653-5p的靶向关系。结果鼻咽癌细胞系(5-8F、6-10B、C666-1)中PRNCR1的表达水平均高于鼻咽上皮细胞NP69(均P<0.001),而miR-653-5p表达水平均低于NP69细胞(均P<0.001)。敲减PRNCR1或过表达miR-653-5p后,鼻咽癌6-10B细胞的增殖能力、划痕愈合率及侵袭细胞数均降低(均P<0.001),而凋亡率升高(均P<0.001)。双荧光素酶报告基因实验证实PRNCR1与miR-653-5p存在靶向关系。敲减PRNCR1后,6-10B细胞中miR-653-5p的表达水平升高(P<0.001)。敲减miR-653-5p可逆转敲减PRNCR1对鼻咽癌6-10B细胞增殖、凋亡、迁移和侵袭的影响。结论PRNCR1在鼻咽癌细胞系中高表达,敲减PRNCR1表达可抑制鼻咽癌细胞增殖、迁移和侵袭,促进细胞凋亡,其作用机制可能与靶向负调控miR-653-5p有关。ObjectiveTo investigate the effect of long non-coding RNA(lncRNA)PRNCR1 on the malignant biological behavior of nasopharyngeal carcinoma cells and its possible mechanism.MethodsThe expressions of PRNCR1 and miR-653-5p in the Nasopharyngeal carcinoma cell lines(5-8 F,6-10 B,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 6-10 B 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.ResultsThe expression level of PRNCR1 in nasopharyngeal carcinoma cell lines(5-8 F,6-10 B,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 6-10 B 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-653-5 p.After knocking down PRNCR1,the expression level of miR-653-5 p in 6-10 B cells was increased(P<0.001).Knocking down miR-653-5p couldreverse the effect of knocking down PRNCR1 on the proliferation,apoptosis,migration and invasion of nasopharyngeal carcinoma 6-10 B 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.

关 键 词：鼻咽癌 PRNCR1 miR-653-5p 细胞增殖 凋亡 迁移 侵袭 

分 类 号：R737.9[医药卫生—肿瘤]