RNA结合基元蛋白24通过调控HOTAIR表达抑制鼻咽癌细胞增殖

Inhibition of nasopharyngeal carcinoma proliferation by RBM24 via regulation of HOTAIR

目的:探讨RNA结合基元蛋白24(RBM24)抑制鼻咽癌细胞增殖的可能机制。方法:分别在永生化鼻咽上皮细胞N5、NP69和鼻咽癌细胞CNE1中转染RBM24 siRNA构建敲低RBM24表达的细胞模型。建模后分别于1~5 d用CCK-8法检测细胞增殖活性,用实时荧光PCR法检测细胞HOX转录反义RNA(HOTAIR)的表达水平。结果:实时荧光PCR法检测结果表明敲低RBM24表达的细胞模型构建成功。第4天时RBM24敲低组的CNE1、N5细胞增殖率(分别为5.11±0.03和2.09±0.18)与相应的对照组细胞(分别为4.53±0.05和1.73±0.12)相比均升高(P均<0.05),且CNE1、N5细胞的HOTAIR m RNA表达水平(分别为67.54±1.87和7.81±1.90)较相应的对照组(1.00±0.21和1.00±0.19)亦升高,差异均有统计学意义(P均<0.05),而NP69细胞的增殖率和HOTAIR mRNA表达水平变化不明显(P均>0.05)。结论:RBM24可抑制鼻咽癌CNE1细胞和永生化鼻咽上皮N5细胞的增殖,其机制可能是通过抑制HOTAIR表达起作用。

OBJECTIVE:This study aimed to explore mechanisms of RBM24 in inhibition of proliferation in nasopharyngeal carcinoma cells.METHODS:Cell models with RBM24 knocked down were built via RBM24 siRNA transfection into immortalized nasopharyngeal epithelial cells N5,NP69,and nasopharyngeal carcinoma cells CNE1.After the cell models was built,CCK-8 assay was performed to evaluate the effect of transfection on cell proliferation each day from day 1 to 5.Real-time PCR was carried out to evaluate the expression of HOTAIR.RESULTS:Successful modeling of RBM24 knocked down were confirmed by real-time PCR.The knockdown significantly induced proliferation of CNE1(5.11±0.03)and N5(2.09±0.18),compared with the control group(4.53±0.05 and 1.73±0.12,respectively).It also upregulated HOTAIR expression in CNE1(67.54±1.87)and N5(7.81±1.90),compared with the control group(1.00±0.21 and 1.00±0.19,respectively,all with P<0.05).But it had no obvious effect on the proliferation and HOTAIR expression in NP69(all with P>0.05).CONCLUSION:RBM24 inhibited cell proliferation of nasopharyngeal carcinoma cell CNE1 and immortalized nasopharyngeal epithelial cells N5,through downregulation of HOTAIR expression.