Orthopeadic Surgery, The Third People's Hospital of Qingdao, Qingdao, Shandong, China.
Internal Medicine-Neurology, The Third People's Hospital of Qingdao, Qingdao, Shandong, China.
Kaohsiung J Med Sci. 2020 Nov;36(11):885-894. doi: 10.1002/kjm2.12261. Epub 2020 Jul 9.
The dysregulation of miR-532-5p is involved in the development of several cancers. Nevertheless, the roles of miR-532-5p in osteosarcoma (OS) have yet to be illuminated. In the present study, we found that miR-532-5p was significantly downregulated in both OS tissues and cell lines. The low level of miR-532-5p was associated with advance clinical stage and poor overall survival in patient with OS. The functional experiments implied that upregulation of miR-532-5p restrained OS U2OS cell growth and metastatic ability in vitro; induced apoptosis, and impaired OS cell growth in vivo. Mechanistically, chemokine (C-X-C Motif) ligand 2 (CXCL2) was proved as a target gene of miR-532-5p. The inhibitory effects of miR-532-5p on OS cell were rescued by CXCL2 overexpression. Altogether, we demonstrated that miR-532-5p exerted tumor-inhibitory functions in OS cell via regulating CXCL2.
miR-532-5p 的失调与几种癌症的发生发展有关。然而，miR-532-5p 在骨肉瘤（OS）中的作用仍有待阐明。在本研究中，我们发现 miR-532-5p 在 OS 组织和细胞系中均显著下调。miR-532-5p 水平低与 OS 患者的临床分期较晚和总体生存率差相关。功能实验表明，miR-532-5p 的上调抑制了 OS U2OS 细胞的体外生长和转移能力；诱导细胞凋亡，并抑制 OS 细胞的体内生长。在机制上，趋化因子（C-X-C 基序）配体 2（CXCL2）被证明是 miR-532-5p 的靶基因。过表达 CXCL2 可挽救 miR-532-5p 对 OS 细胞的抑制作用。总之，我们证明 miR-532-5p 通过调节 CXCL2 发挥抑制 OS 细胞的肿瘤抑制功能。
