Wang Xuan, Yang Ji-Yuan, Cai Jun, Zhang De-Jun, Zhao Lei, Luo Li-Hua, Xiong Ying, Zhang Tao, Jin Min
Department of Oncology, First Affiliated Hospital of Yangtze University Jingzhou 434000, Hubei, China.
Wuhan Pulmonary Hospital, Wuhan Institute for Tuberculosis Control Wuhan 430030, China.
Am J Transl Res. 2021 Feb 15;13(2):617-631. eCollection 2021.
MiR-543 and Numb are associated with various malignancies, including prostate cancer (PCa). However, whether miR-543 regulates Numb in PCa development remains unclear. In this study, we identified Numb as a direct target of miR-543. The role of miR-543 was examined both in vitro and in vivo. The in vivo effects of miR-543 were investigated using tumor transplantation experiments and a lung metastasis model. The in vitro effects of miR-543 on proliferation, migration, invasion, and cancer stem-like cell (CSC)-associated properties were also examined. The binding sites of Numb were predicted using bioinformatics tools and confirmed by luciferase and rescue assays. QRT-PCR and western blot analyses were used to detect target expression levels. Expression levels of both miR-543 and Numb were manipulated in CD44+ and CD44-PCa cells followed by a series of functional assays. The results demonstrated that miR-543 promoted PCa growth and metastasis both in vivo and in vitro. Luciferase reporter assays, qRT-PCR, and western blot analyses revealed Numb as a direct target of miR-543. The function of miR-543 was abolished by Numb, as shown in rescue experiments. Moreover, miR-543 was verified to promote CSC properties, whereas Numb elicited the opposite effects. MiR-543 also influenced the expression of several stem-like factors, including Dll4, NF-κB, c-myc, and Oct-4, and the Numb/p53 signaling pathway. Taken together, these results demonstrate that miR-543 plays an oncogenic role by negatively controlling Numb, revealing the existence of an miR-543/Numb/p53 regulatory pathway in PCa tumorigenesis and development.
微小RNA-543(miR-543)和NUMB与包括前列腺癌(PCa)在内的多种恶性肿瘤相关。然而,miR-543在PCa发生发展过程中是否调控NUMB仍不清楚。在本研究中,我们确定NUMB是miR-543的直接靶点。我们在体外和体内研究了miR-543的作用。利用肿瘤移植实验和肺转移模型研究了miR-543的体内作用。还检测了miR-543在体外对增殖、迁移、侵袭以及癌症干细胞样细胞(CSC)相关特性的影响。使用生物信息学工具预测NUMB的结合位点,并通过荧光素酶和拯救实验进行验证。采用实时定量聚合酶链反应(QRT-PCR)和蛋白质免疫印迹分析来检测靶点表达水平。在CD44 +和CD44 - PCa细胞中调控miR-543和NUMB的表达水平,随后进行一系列功能实验。结果表明,miR-543在体内和体外均促进PCa的生长和转移。荧光素酶报告基因实验、qRT-PCR和蛋白质免疫印迹分析显示NUMB是miR-543的直接靶点。拯救实验表明,NUMB消除了miR-543的功能。此外,证实miR-543促进CSC特性,而NUMB则产生相反作用。miR-543还影响包括Dll4、核因子κB(NF-κB)、原癌基因c-myc和八聚体结合转录因子4(Oct-4)在内的几种干细胞样因子的表达以及NUMB/p53信号通路。综上所述,这些结果表明miR-543通过负向调控NUMB发挥致癌作用,揭示了PCa肿瘤发生发展过程中存在miR-543/NUMB/p53调控通路。