Abstract
Objective: To investigate the role of miR-181a in promoting the proliferation and metastasis of osteosarcoma cells by targeting RASSF1A. Methods: The level of miR-181a in 30 human osteosarcoma tissues and corresponding bone tissues was detected by real-time PCR, and the correlation between the level of miR-181a and clinicopathological characteristics of osteosarcoma was analyzed. Osteosarcoma cells MG-63 were transfected with chemically-synthesized miR-181a mimics and inhibitors, and the proliferation, migration and invasion of MG-63 cells were detected by MTT and Transwell assay. The specific binding ability of miR-181a to RASSF1A 3'-UTR was theoretically predicted and detected by the dual luciferase reporter gene assay. Results: The level of miR-181a in osteosarcoma tissues was statistically higher than that in the corresponding bone tissues (P<0.001). However, the level of miR-181a was not correlated with gender, age, tumor size and stage (P>0.05). MTT and Transwell assays showed that the growth rate, migration and invasion ability of MG-63 cells with up-regulation of miR-181a was significantly increased compared with negative control (P<0.05), while the growth rate, migration and invasion ability of MG-63 with down-regulated miR-181a was significantly decreased compared with negative control (P<0.05). Luciferase reporter gene assay showed that miR-181a targeted the 3'-UTR of RASSF1A and regulated the expression of RASSF1A. Conclusion: MiR-181a promotes the proliferation and metastasis of osteosarcoma cells through specifically binding to RASSF1A 3'-UTR and subsequent down-regulation of RASSF1A.
| Translated title of the contribution | miR-181a promotes the proliferation and metastasis of osteosarcoma cells by targeting RASSF1A |
|---|---|
| Original language | Chinese (Traditional) |
| Pages (from-to) | 789-795 |
| Number of pages | 7 |
| Journal | Journal of Central South University (Medical Sciences) |
| Volume | 41 |
| Issue number | 8 |
| DOIs | |
| State | Published - 27 Aug 2016 |
| Externally published | Yes |