Guo Xinzhen, Zhang Jie, Pang Jianfeng, He Sheng, Li Guojun, Chong Yang, Li Chao, Jiao Zhijian, Zhang Shiqian, Shao Ming
Department of Orthopedic Surgery, The First Affiliated Hospital of Harbin Medical University, No. 23, You Zheng St., Nangang District, Harbin, Heilongjiang Prov., 150001, China.
Ming Shui County People's Hospital, Suihua, Heilongjiang Prov., 150001, China.
Tumour Biol. 2016 Jul;37(7):9181-7. doi: 10.1007/s13277-016-4797-4. Epub 2016 Jan 14.
Deregulated expression of miRNAs contributes to the development of osteosarcoma. Our previous study has showed that miR-503 was downregulated in osteosarcoma tissues. However, the mechanism of the miR-503 in osteosarcoma development still remains largely undefined. In our study, we found that miR-503 overexpression suppressed cell invasion and migration and inhibited epithelial-to-mesenchymal transition (EMT) of MG-63. Furthermore, we identified that c-myb, an oncogene, was a direct target of miR-503. Moreover, overexpression of c-myb could rescue miR-503-suppressed invasion and EMT. The expression of c-myb was upregulated in osteosarcoma cell lines. Therefore, we conclude that high miR-503 expression suppressed osteosarcoma cell mobility and EMT through targeting c-myb, and this may serve as a therapeutic target.
微小RNA(miRNA)的表达失调促进骨肉瘤的发展。我们之前的研究表明,miR-503在骨肉瘤组织中表达下调。然而,miR-503在骨肉瘤发展中的作用机制仍在很大程度上不明确。在我们的研究中,我们发现miR-503过表达抑制MG-63细胞的侵袭和迁移,并抑制其上皮-间质转化(EMT)。此外,我们确定原癌基因c-myb是miR-503的直接靶点。而且,c-myb过表达可以挽救miR-503抑制的侵袭和EMT。c-myb在骨肉瘤细胞系中表达上调。因此,我们得出结论,高表达的miR-503通过靶向c-myb抑制骨肉瘤细胞的迁移能力和EMT,这可能成为一个治疗靶点。