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miR-485-5p 通过靶向 CX3CL1 抑制骨肉瘤的转移和增殖。

MiR-485-5p inhibits metastasis and proliferation of osteosarcoma by targeting CX3CL1.

机构信息

Department of Trauma Emergency Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Ji'nan, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Nov;22(21):7197-7204. doi: 10.26355/eurrev_201811_16253.

Abstract

OBJECTIVE

To investigate the potential effect of miR-485-5p on the development of osteosarcoma (OA) and its relevant mechanism.

PATIENTS AND METHODS

The expression level of miR-485-5p was detected in OA tissues and cells (MG-63) comparing with corresponding adjacent normal tissues and normal human osteoblastic cell lines (Hfob1.19), respectively. Luciferase assay was performed to evaluate the interaction between miR-485-5p and CX3CL1, the effects of miR-485-5p on MG-63 cells were determined by subsequent experiments including cell proliferation, expression level of CX3CL1, detection of invasion and migration capacities.

RESULTS

In our present research, miR-485-5p was down-regulated in OA tissues and we got the same result in OA cells. In order to obtain potential target of miR-485-5p, we checked it in three publicly available algorithms, TargetScan, miRDB and microRNA. We found that CX3CL1 is a direct target of miR-485-5p, and Luciferase assays confirmed our hypothesis. The results showed that decreased expression of CX3CL1 resulting from the up-regulation of miR-485-5p could decelerate cell proliferation, invasion and migration in OA cells.

CONCLUSIONS

We showed the suppressor function of miR-485-5p in OA by targeting CX3CL1, indicating that miR-485-5p/CX3CL1 axis might be a potential therapeutic target for the treatment of OA.

摘要

目的

探讨 miR-485-5p 对骨肉瘤(OA)发展的潜在影响及其相关机制。

方法

分别检测 OA 组织和细胞(MG-63)与相应相邻正常组织和正常人成骨细胞系(Hfob1.19)中 miR-485-5p 的表达水平。通过荧光素酶实验评估 miR-485-5p 与 CX3CL1 之间的相互作用,随后通过实验确定 miR-485-5p 对 MG-63 细胞的影响,包括细胞增殖、CX3CL1 的表达水平、侵袭和迁移能力的检测。

结果

在本研究中,miR-485-5p 在 OA 组织中下调,我们在 OA 细胞中也得到了相同的结果。为了获得 miR-485-5p 的潜在靶标,我们在三个公开可用的算法(TargetScan、miRDB 和 microRNA)中进行了检查。我们发现 CX3CL1 是 miR-485-5p 的直接靶标,荧光素酶实验证实了我们的假设。结果表明,miR-485-5p 上调导致 CX3CL1 表达降低,可减缓 OA 细胞的增殖、侵袭和迁移。

结论

我们通过靶向 CX3CL1 显示了 miR-485-5p 在 OA 中的抑制作用,表明 miR-485-5p/CX3CL1 轴可能是治疗 OA 的潜在治疗靶点。

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