甲基转移酶蛋白16对前列腺癌细胞株22RV1细胞迁移功能的影响  

Effect of methyltransferase like protein 16 on migration ability of prostate cancer cell line 22RV1 cells

作　　者：张磊[1] 华立新[1] 成功[1] Zhang Lei;Hua Lixin;Cheng Gong(Department of Urology,the First Affiliated Hospital,Nanjing Medical University,Nanjing 210029,China)

机构地区：[1]南京医科大学附属第一医院泌尿外科,210029

出　　处：《中华实验外科杂志》2020年第2期290-292,共3页Chinese Journal of Experimental Surgery

摘　　要：目的观察甲基转移酶蛋白16(METTL16)在前列腺癌组织和细胞株中的表达,探讨METTL16对人前列腺癌细胞株(22RV1)细胞功能的影响。方法实时定量反转录-聚合酶链反应(RT-qPCR)检测METTL16在前列腺癌组织(取自南京医科大学第一附属医院泌尿外科行根治性前列腺切除患者)和细胞中的表达。22RV1细胞株稳定转染相关慢病毒。以RT-qPCR以及蛋白质印迹法(Western blot)检测在22RV1细胞中过表达或敲低METTL16的效率。以细胞迁移实验检测22RV1细胞迁移能力的改变。测定的数值通过统计分析软件SPSS 21.0,采用t检验。结果在前列腺癌组织、LNCaP细胞株以及22RV1细胞株中,METTL16在mRNA水平的都呈现出过表达的趋势[癌组织为1.00±0.43,癌旁组织为2.12±0.68,t=-5.405,P<0.05;人正常前列腺基质永生化细胞(WPMY-1)为1.00±0.17,22RV1为2.16±0.93,t=-8.568,P<0.05;LNCaP为1.51±0.17,t=-3.073,P<0.05],差异均有统计学意义;而在蛋白水平,LNCaP细胞株以及22RV1细胞株的METTL16依旧呈现高表达的趋势(WPMY-1为1.00±0.23,22RV1为2.91±0.85,t=-3.038,P<0.05;LNCaP为1.99±0.43,t=-2.896,P<0.05),差异均有统计学意义。在22RV1细胞中过表达METTL16后导致细胞迁移能力的增强[相对细胞量为过表达空载体组(ON-22RV1)为1.00±0.04,过表达METTL16组(OE-22RV1)为3.18±0.10,t=-34.951,P<0.05]而敲低METTL16则导致相反结果(相对细胞量:SCR-22RV1为1.00±0.06,sh1-22RV1为0.47±0.06,t=3.862,P<0.05;sh2-22RV1为0.64±0.05,t=9.200,P<0.05),差异均有统计学意义。结论METTL16在前列腺癌的生理过程中可能起原癌基因的作用,并且调控着细胞的迁移能力。Objective To observe the expression of YTH N6-methyladenosine RNA binding protein 2(METTL16)in prostate cancer tissues and prostate cancer cells and study the effect of METTL16 on the function of 22RV1 cells.Methods The expression of METTL16 in prostate cancer tissues and 22RV1 cells was detected by real-time quantitative reverse transcriptase-polymerase chain reaction(RT-qPCR).22RV1 cells were stably transfected with lentivirus approach.The efficiency of over-expressing or knocking-down of METTL16 in 22RV1 cells was tested by RT-qPCR and Western blotting.Cell migration assay was used to analyze the change of the migration ability of 22RV1 cells.Results The mRNA level of METTL16 was up-regulated in prostate cancer tissues and LNCaP and 22RV1 cells(cancer tissues:1.00±0.43;paired adjacent non-cancerous tissues:2.12±0.68,t=-5.405,P<0.05;WPMY-1:1.00±0.17;22RV1:2.16±0.93,t=-8.568,P<0.05.LNCaP:1.51±0.17,t=-3.073,P<0.05),and the protein level of METTL16 was also up-regulated in LNCaP and 22RV1 cells(WPMY-1:1.00±0.23;22RV1:2.91±0.85,t=-3.038,P<0.05.LNCaP:1.99±0.43,t=-2.896,P<0.05).The over-expression of METTL16 in 22RV1 cells led to an enhancement of the migration ability(relative cell number,for over-expressive negative control(ON)-22RV1:1.00±0.04;for over-expressive(OE)-22RV1:3.18±0.10,t=-34.951,P<0.05),while the knocking-down of METTL16 in 22RV1 cells showed an opposite effect(relative cell number,for scramble control(SCR)-22RV1:1.00±0.06;for sh1-22RV1:0.47±0.06,t=3.862,P<0.05;for sh2-22RV1:0.64±0.05,t=9.200,P<0.05).Conclusion METTL16 could act as an oncogene in prostate cancer physiological process and regulate the migration ability of prostate cancer cells.

关 键 词：N6-甲基腺嘌呤 前列腺癌 迁移 

分 类 号：R737[医药卫生—肿瘤]