Department of Orthopedics, Jingzhou Central Hospital, Jingzhou, Hubei Province, P.R. China.
The First People's Hospital of Jingzhou, Jingzhou, Hubei Province, P.R. China.
Oncol Res. 2019 Feb 5;27(2):157-163. doi: 10.3727/096504018X15190861873459. Epub 2018 Feb 22.
miR-363-3p has been shown to suppress tumor growth and metastasis in various human cancers. However, the function of miR-363-3p in osteosarcoma (OS) has not been determined. In our study, we found that the expression of miR-363-3p was significantly downregulated in OS tissues compared with adjacent normal tissues. miR-363-3p expression was associated with the poor overall survival rate of OS patients. Moreover, we found that overexpression of miR-363-3p markedly inhibited the proliferation, migration, and invasion of U2OS and MG63 cells. Moreover, we found that SOX4 was a direct target of miR-363-3p in OS cells. Overexpression of miR-363-3p significantly inhibited the expression of SOX4. Expression levels of miR-363-3p and SOX4 were negatively correlated in OS tissues. Finally, we found that restoration of SOX4 attenuated the suppressive effects of miR-363-3p on the proliferation, migration, and invasion of U2OS and MG63 cells. Therefore, our findings demonstrated that miR-363-3p served as a tumor suppressor in OS tissues by targeting SOX4.
miR-363-3p 已被证明可抑制多种人类癌症的肿瘤生长和转移。然而,miR-363-3p 在骨肉瘤 (OS) 中的功能尚未确定。在我们的研究中,我们发现 miR-363-3p 的表达在 OS 组织中明显低于相邻的正常组织。miR-363-3p 的表达与 OS 患者的总生存率降低有关。此外,我们发现 miR-363-3p 的过表达可显著抑制 U2OS 和 MG63 细胞的增殖、迁移和侵袭。此外,我们发现 SOX4 是 OS 细胞中 miR-363-3p 的直接靶标。miR-363-3p 的过表达显著抑制了 SOX4 的表达。OS 组织中 miR-363-3p 和 SOX4 的表达水平呈负相关。最后,我们发现恢复 SOX4 减弱了 miR-363-3p 对 U2OS 和 MG63 细胞增殖、迁移和侵袭的抑制作用。因此,我们的研究结果表明,miR-363-3p 通过靶向 SOX4 作为 OS 组织中的肿瘤抑制因子发挥作用。