miR-432-3p靶向ELK1调控甲状腺癌细胞SW579的凋亡  

miR-432-3p targets ELK1 to regulate the apoptosis of thyroid cancer cell SW579

作　　者：张馨月 刘地发 李春香 邵春燕 葛春霞 ZHANG Xin-yue;LIU Di-fa;LI Chun-xiang;SHAO Chun-yan;GE Chun-xia(Department of Hematology and Oncology,Haian People's Hospital,Haian 220060,China)

机构地区：[1]江苏省海安市人民医院血液肿瘤科,江苏海安220060

出　　处：《生物技术》2022年第4期451-458,437,共9页Biotechnology

摘　　要：[目的]探讨甲状腺癌细胞SW579中PTEN通路调控细胞凋亡的潜在机制。[方法]免疫组织化学和实时荧光定量PCR检测PTEN在甲状腺癌组织和癌旁组织中的表达水平。过表达PTEN后,检测甲状腺癌细胞SW579凋亡水平。通过启动子区域转录因子预测后筛选甲状腺癌细胞SW579中调控PTEN的转录因子。通过miRDB数据库在线分析和实时荧光定量PCR鉴定转录因子的miRNA。过表达或敲低miRNA,检测甲状腺癌细胞SW579的凋亡水平。[结果]PTEN在甲状腺癌组织中的蛋白和mRNA表达水平小于癌旁组织。在甲状腺癌细胞SW579中过表达PTEN后,甲状腺癌细胞SW579的凋亡水平上升(P<0.05)。敲低EGR1后,PTEN的表达水平下降(P<0.05);敲低ELK1后,PTEN的表达水平上升(P<0.05)。EGR1在甲状腺癌组织中mRNA和蛋白的表达水平低于癌旁组织(P<0.05)。ELK1在甲状腺癌组织中mRNA和蛋白的表达水平高于癌旁组织(P<0.05)。敲低ELK1后,EGR1的mRNA表达水平显著上升(P<0.05)。干扰miR-432-3p后,ELK1的mRNA和蛋白表达水平上升(P<0.05),ERG1和PTEN的蛋白表达水平下降(P<0.05),甲状腺癌细胞SW579的凋亡水平显著下降(P<0.05)。过表达miR-432-3p后,ELK1的mRNA和蛋白表达水平下降(P<0.05),ERG1和PTEN的蛋白表达水平上升(P<0.05),甲状腺癌细胞SW579的凋亡水平上升(P<0.05)。[结论]miR-432-3p通过靶向ELK1 mRNA 3’端非编码区,抑制ELK1的mRNA和蛋白表达水平,增加转录因子ERG1的转录,提升了PTEN蛋白的表达,最终促进了甲状腺癌细胞SW579的凋亡水平。[Objective]To investigate the potential mechanism of PTEN pathway regulating cell apoptosis in thyroid cancer cell SW579.[Method]Immunohistochemistry and real-time quantitative PCR were used to detect the expression of PTEN in thyroid carcinoma and paracancer tissues.After overexpression of PTEN,apoptosis level of thyroid cancer cell SW579 was detected.Transcriptional factors that regulate PTEN in thyroid cancer cell SW579 were screened by promoter region transcriptional factors prediction.miRNA of transcription factors were identified by online analysis of miRDB database and real-time fluorescence quantitative PCR.The apoptosis level of thyroid cancer cell SW579 was detected by overexpression or knockdown of miRNA.[Result]The protein and mRNA expression levels of PTEN in thyroid cancer tissues were lower than those in para-cancer tissues.After overexpression of PTEN in thyroid cancer cell SW579,the apoptosis level of thyroid cancer cell SW579 increased(P<0.05).After EGR1 knockdown,the expression level of PTEN decreased(P<0.05).After ELK1 knockdown,the expression level of PTEN increased(P<0.05).The mRNA and protein expression levels of EGR1 in thyroid cancer tissues were lower than those in adjacent tissues(P<0.05).The mRNA and protein expression levels of ELK1 in thyroid carcinoma tissues were higher than those in adjacent tissues(P<0.05).After ELK1 knockdown,EGR1 mRNA expression level was significantly increased(P<0.05).After miR-432-3p was interfered,the mRNA and protein expression levels of ELK1 were increased(P<0.05),the protein expression levels of ERG1 and PTEN were decreased(P<0.05),and the apoptosis level of thyroid cancer cell SW579 was significantly decreased(P<0.05).After overexpression of miR-432-3p,the mRNA and protein expression levels of ELK1 were decreased(P<0.05),the protein expression levels of ERG1 and PTEN were increased(P<0.05),and the apoptosis level of thyroid cancer cell SW579 was increased(P<0.05).[Conclusion]miR-432-3p targets the non-coding region at the 3 end of ELK1 mRNA,inhibits the

关 键 词：miR-432-3p ELK1 甲状腺癌 SW579 PTEN 凋亡 

分 类 号：R736.1[医药卫生—肿瘤]