F-R Wang1, S-H Xu, B-M Wang, F Wang. 1. Department of Trauma Emergency Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Ji'nan, China. 15168887120@163.com.
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.
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.