长链非编码RNA SNHG16通过微小RNA-455-3p/Nocth2对鼻咽癌细胞增殖、凋亡和周期的影响

Effect of long non-coding RNA SNHG16 on proliferation,apoptosis and cycle of nasopharyngeal carcinoma cells through microRNA-455-3p/Nocth2

目的探讨长链非编码RNA(lncRNA)SNHG16通过微小RNA(miR)-455-3p/Nocth2对鼻咽癌细胞增殖、凋亡和周期的影响及其机制。方法选取2017年6月到2021年6月新乡市中心医院收治的51例鼻咽癌及其癌旁组织作为研究对象,采用荧光定量聚合酶链反应(PCR)分析肿瘤组织和癌旁组织lncRNA SNHG16和miR-455-3p表达水平。采用慢病毒建立lncRNA SNHG16敲降稳定细胞系SNHG16 KD组和对照组,采用细胞计数试剂盒(CCK-8)分析两组细胞增殖能力和体内成瘤能力。采用流式细胞术分析两组细胞凋亡水平;采用流式细胞术分析细胞周期变化;采用生物信息学和生物信息学和双荧光素酶报告基因分析lncRNA SNHG16靶基因。组间数据比较采用t检验。结果癌旁组织lncRNA SNHG16表达水平(0.89±0.09)明显低于鼻咽癌组织lncRNA SNHG16表达水平(2.11±0.22),差异有统计学意义(t=36.260,P<0.05)。对照组细胞吸光度(A)值(1.93±0.06)明显高于SNHG16 KD组(1.27±0.06),差异有统计学意义(t=18.350,P<0.05)。对照组细胞在裸鼠体内成瘤体积[(904.94±39.53)mm^(3)]明显高于SNHG16 KD组细胞成瘤体积[(742.82±97.80)mm^(3)],差异有统计学意义(t=4.860,P<0.05)。对照组细胞成瘤重量[(4.70±0.46)g]明显高于SNHG16 KD组细胞[(2.22±0.18)g],差异有统计学意义(t=15.960,P<0.05)。对照组细胞凋亡比例[(4.07±1.34)%]明显低于SNHG16 KD组细胞[(26.79±5.16)%],差异有统计学意义(t=10.430,P<0.05)。对照组细胞G0/G1期比例[(31.56±3.27)%]明显高于SNHG16 KD组细胞[(45.96±1.72)%],差异有统计学意义(t=9.5201,P<0.05)。lncRNA SNHG16是miR-455-3p的海绵。对照组细胞miR-455-3p表达水平(1.19±0.10)明显低于SNHG16 KD组细胞(2.15±0.15),差异有统计学意义(t=13.040,P<0.05)。对照组细胞Notch2表达水平(0.93±0.05)明显高于SNHG16 KD组细胞(0.44±0.06),差异有统计学意义(t=13.040,P<0.05)。结论lncRNA SNHG16海绵吸附miR-455-3p,进而调控Nocth2表达水平,调节鼻咽癌细胞增殖、凋亡和周期。

Objective To investigate the effect of long non-coding RNA(lncRNA)SNHG16 on proliferation,apoptosis and cell cycle of nasopharyngeal carcinoma cells through microRNA(miR)-455-3p/Nocth2 and its molecular mechanism.Methods 51 cases of nasopharyngeal carcinoma and their adjacent tissues treated in our hospital from June 2017 to June 2021 were selected as the study subjects.The expression levels of lncRNA SNHG16 and miR-455-3p in tumor tissues and adjacent tissues were analyzed by fluorescence quantitative polymerase chain reaction(PCR).The lncRNA SNHG16 knockdown stable cell lines SNHG16 KD group and control group were established by lentivirus,and the cell proliferation and tumorigenesis in vivo of the two groups were analyzed by cell counting kit-8(CCK-8).The level of apoptosis and cell cycle were analyzed in the two groups by flow cytometry.LncRNA SNHG16 target genes were analyzed using bioinformatics and bioinformatics and dual luciferase reporter genes.T test was used to compare the data between groups.Results The expression level of lncRNA SNHG16 in adjacent tissues(0.89±0.09)was significantly lower than that in nasopharyngeal carcinoma tissues(2.11±0.22,t=36.260,P<0.05).The absorbance(a)of cells in the control group(1.93±0.06)was significantly higher than that in the SNHG16 KD group(1.27±0.06,t=18.350,P<0.05).The tumor formation volume of the control group cells in nude mice[(904.94±39.53)mm^(3)]was significantly higher than that of the SNHG16 KD group cells[(742.82±97.80)mm^(3),t=4.860,P<0.05].The tumorigenic weight of cells in the control group[(4.70±0.46)g]was significantly higher than that of cells in the SNHG16 KD group[(2.22±0.18)g,t=15.960,P<0.05].The percentage of apoptosis in the control group[(4.07±1.34)%]was significantly lower than that in the SNHG16 KD group[(26.79±5.16)%,t=10.430,P<0.05].The G0/G1 phase ratio of cells in the control group[(31.56±3.27)%]was significantly higher than that in the snhg16 KD Group[(45.96±1.72)%,t=9.5201,P<0.05].LncRNA SNHG16 is a sponge of miR-455-3p.The expression level of miR-455-3p in control group(1.19±0.10)was significantly lower than that in SNHG16 KD group(2.15±0.15,t=13.040,P<0.05).The expression level of Notch2 in control group(0.93±0.05)was significantly higher than that in SNHG16 KD group(0.44±0.06,t=13.040,P<0.05).Conclusion LncRNA SNHG16 as a sponge of miR-455-3p,regulates the expression level of nocth2 and regulates the proliferation,apoptosis and cycle of nasopharyngeal carcinoma cells.