RNA结合基元蛋白24通过调控HOTAIR表达抑制鼻咽癌细胞增殖

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 mRNA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。

Inhibition of nasopharyngeal carcinoma proliferation by RBM24 via regulation of HOTAIR

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.