miR-106b-5p 3'-末端2'-O-甲基化对乳腺癌细胞的影响  

Effect of 3'-terminal 2'-O-methylation of miR-106b-5p on breast cancer cells

作　　者：李双健[1] 李丹[1] 丰锦春 李宇翔 迪力夏提·金斯汗[1] 赵倩[1] LI Shuang-jian;LI Dan;FENG Jin-chun;LI Yu-xiang;Dilixiati Jinsihan;ZHAO Qian(Department of Breast Surgery,Affiliated Tumor Hospital of Xinjiang Medical University,Urumqi 830000,China)

机构地区：[1]新疆医科大学附属肿瘤医院乳腺外科,新疆乌鲁木齐830000

出　　处：《生物技术》2023年第5期586-591,550,共7页Biotechnology

基　　金：新疆自然科学基金项目(2017D01C379)。

摘　　要：[目的]探讨miR-106b-5p的3'-末端2'-O-甲基化修饰在乳腺癌细胞中的影响。[方法]纳入2019年9月-2021年9月收治的乳腺癌患者,收集其乳腺癌组织和癌旁组织。敲低或过表达miR-106b-5p后,检测乳腺癌细胞的增值水平。乳腺癌和癌旁组织中纯化的miR-106b-5p进行质谱分析以确定分子质量和LC-MS/MS确定核苷修饰。分析甲基转移酶HENMT1对miR-106b-5p的3'-末端2'-O-甲基化作用。[结果]敲低miR-106b-5p后,乳腺癌细胞的增值水平下降(P<0.05)。乳腺组织中miR-106b-5p的3'-末端2'-O-甲基化显著高于癌旁中的水平(P<0.05)。敲低HENMT1后,乳腺癌细胞MCF7中miR-106b-5p的3'-末端2'-O-甲基化水平下降(P<0.05)。敲低HENMT1后,miR-106b-5p的半衰期下降(P<0.05)。[结论]HENMT1能对miR-106b-5p进行3'-末端2'-O-甲基化修饰(65.32±16.40 vs 11.49±3.20)。3'-末端2'-O-甲基化能提升miR-106b-5p的半衰期(0.79±0.05 vs 0.98±0.07)并促进miR-106b-5p的促乳腺癌细胞增殖(1.70±0.08 vs 1.04±0.06)。[Objective]To investigate the effect of 3'-terminal 2'-O-methylation modification of miR-106b-5p on breast cancer cells.[Method]Breast cancer patients admitted to our hospital from September 2019 to September 2021 were included,and their breast cancer tissues and paracancerous tissues were collected.After knockdown or overexpression of miR-106b-5p,the value-added level of breast cancer cells was detected.Purified miR-106b-5p from breast cancer and paraneoplastic tissues were subjected to mass spectrometry to determine molecular mass and LC-MS/MS to determine nucleoside modifications.The 3'-terminal 2'-O-methylation of miR-106b-5p by the methyltransferase HENMT1 was analyzed.[Result]The value-added level of breast cancer cells decreased after knockdown of miR-106b-5p(P<0.05).The 3'-terminal 2'-O-methylation of miR-106b-5p in breast tissues was significantly higher than that in the paracancer(P<0.05).The 3'-terminal 2'-O-methylation level of miR-106b-5p in MCF7 of breast cancer cells decreased after knockdown of HENMT1(P<0.05).The half-life of miR-106b-5p decreased after knockdown of HENMT1(P<0.05).[Conclusion]HENMT1 modifies 3'-terminal 2'-O-methylation of miR-106b-5p(65.32±16.40 vs 11.49±3.20).3'-terminal 2'-O-methylation enhances the half-life of miR-106b-5p(0.79±0.05 vs 0.98±0.07)and promotes miR-106b-5p pro-breast cancer cell proliferation(1.70±0.08 vs 1.04±0.06).

关 键 词：miR-106b-5p 3'-末端2'-O-甲基化 乳腺癌 增殖 HENMT1 

分 类 号：R737.9[医药卫生—肿瘤]