miR-659-3p靶向CTNNBIP1调控甲状腺癌细胞凋亡的机制  

Mechanism of miR-659-3p targeting CTNNBIP1 to regulate the apoptosis of thyroid cancer cells

作　　者：张军[1] 彭大伟 李鸽姿 李杰[1] 李杏 陈嘉丽 吴淑宁 ZHANG Jun;PENG Da-wei;LI Ge-zi;LI Jie;LI Xing;CHEN Jia-li;WU Shu-ning(Department of Thyroid and Breast Surgery,Shenzhen Hospital,Second Xiangya Hospital,Central South University,Shenzhen 518000,China)

机构地区：[1]中南大学湘雅二医院深圳医院(深圳市前海蛇口自贸区医院)甲状腺乳腺外科,深圳广东518000

出　　处：《生物技术》2023年第1期48-54,共7页Biotechnology

摘　　要：[目的]探讨miR-659-3p在甲状腺癌细胞中的潜在功能和机制。[方法]纳入甲状腺乳头癌患者60例,比较甲状腺患者癌旁组织和癌组织中miR-659-3p的表达水平。过表达或敲低miR-659-3p后检测甲状腺癌细胞TPC-1的增殖水平和凋亡水平,并进行底物鉴定。[结果] miR-659-3p的表达水平在60个甲状腺癌组织中也显著上调(P<0.05)。miR-659-3p敲低后TPC-1的增殖水平显著下降(P<0.05)、 TPC-1的凋亡水平显著上升(P<0.05)。敲低CTNNBIP1时,TPC-1的凋亡水平下降(P<0.05)、 TPC-1的细胞活力水平上升(P<0.05)。过表达miR-659-3p时,CTNNBIP1的蛋白水平和mRNA水平显著下降(P<0.05);敲低miR-659-3p时,CTNNBIP1的蛋白水平和mRNA水平显著上升(P<0.05)。过表达miR-659-3p后,Wnt/β-catenin通路的关键蛋白β-catenin的核定位增多;敲低miR-659-3p后,β-catenin的核定位减少。[结论] miR-659-3p通过靶向CTNNBIP1 mRNA的3′端非编码区减少CTNNBIP1的表达,促进了甲状腺细胞的增殖,抑制了额甲状腺癌细胞的凋亡。[Objective]To investigate the potential function and mechanism of miR-659-3p in thyroid cancer cells.[Method]A total of 60 patients with thyroid papillary carcinoma were enrolled to compare the expression levels of miR-659-3p in para-cancer tissues and cancer tissues of thyroid patients.After overexpression or knockdown of miR-659-3p, the proliferation level and apoptosis level of TPC-1 of thyroid cancer cells were detected, and the substrate was identified.[Result]The expression level of miR-659-3p was also significantly up-regulated in 60 thyroid cancer tissues(P<0.05).After miR-659-3p knockdown, the proliferation level of TPC-1 was significantly decreased(P<0.05),and the apoptosis level of TPC-1 was significantly increased(P<0.05).When CTNNBIP1 was knocked down, the apoptosis level of TPC-1 decreased(P<0.05),and the cell viability level of TPC-1 increased(P<0.05).When miR-659-3p was overexpressed, the protein and mRNA levels of CTNNBIP1 were significantly decreased(P<0.05);when miR-659-3p was knocked down, the protein and mRNA levels of CTNNBIP1 were significantly increased(P<0.05).After overexpression of miR-659-3p, the nuclear localization of β-catenin, a key protein of the Wnt/β-catenin pathway, increased;after knockdown of miR-659-3p, the nuclear localization of β-catenin decreased.[Conclusion] miR-659-3p reduced the expression of CTNNBIP1 by targeting the 3′UTR of CTNNBIP1 mRNA,and it promoted the proliferation of thyroid cells and inhibited the apoptosis of frontal thyroid cancer cells.

关 键 词：miR-659-3p CTNNBIP1 甲状腺癌细胞 凋亡 Β-CATENIN 

分 类 号：Q784[生物学—分子生物学]