Shen Fei, Gan Xiao-Xiong, Deng Xing-Yan, Feng Jian-Hua, Cai Wen-Song, Shen Liang, Xiao Huan-Qing, Xu Bo
Department of Thyroid Surgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Department of Thyroid Surgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, Guangdong 510180, P.R. China.
Oncol Lett. 2020 Nov;20(5):223. doi: 10.3892/ol.2020.12086. Epub 2020 Sep 10.
An increasing amount of evidence has demonstrated the importance of microRNAs (miRNAs/miRs) in the tumorigenesis of malignant types of cancer, and data retrieved from The Cancer Genome Atlas database revealed that miR-3690 was upregulated in thyroid cancer (TC). The present study focused on the biological function and mechanism of miR-3690 in TC, demonstrating that miR-3690 expression was significantly elevated in TC cells and clinical tissues. Functional studies indicated that miR-3690 acted as an oncogene in TC by promoting cell proliferation, colony formation and cell cycle progression in association with the increased expression of cyclin E and c-myc. Mechanistically, prediction software indicated that Dickkopf-related protein 3 (DKK3) was a target of miR-3690, which was confirmed by the results of luciferase reporter assays and western blotting. DKK3 silencing abrogated the functions of miR-3690-in on TC cell proliferation. Collectively, the findings of the present study demonstrated that miR-3690 promoted TC cell proliferation and indicated miR-3690 as a potential biomarker and therapeutic target for TC.
越来越多的证据表明，微小RNA（miRNA/miR）在恶性肿瘤的发生发展中具有重要作用，从癌症基因组图谱数据库检索到的数据显示，miR-3690在甲状腺癌（TC）中上调。本研究聚焦于miR-3690在TC中的生物学功能及机制，结果表明miR-3690在TC细胞和临床组织中的表达显著升高。功能研究表明，miR-3690通过促进细胞增殖、集落形成和细胞周期进程，以及伴随细胞周期蛋白E和c-myc表达增加，在TC中发挥癌基因作用。机制上，预测软件表明Dickkopf相关蛋白3（DKK3）是miR-3690的靶点，荧光素酶报告基因检测和蛋白质印迹结果证实了这一点。DKK3沉默消除了miR-3690对TC细胞增殖的作用。总体而言，本研究结果表明miR-3690促进TC细胞增殖，并提示miR-3690作为TC的潜在生物标志物和治疗靶点。
