miR-205 suppresses the proliferative and migratory capacity of human osteosarcoma MG-63 cells by targeting VEGFA

Abstract

Li Wang, Minhong Shan, Fengyi Yang, Yang Liu, Hongxia Qi, Lijuan Zhou, Lirong Qiu, Yanshuang Li Department of Operating Room 1, Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, People’s Republic of China Background: Osteosarcoma (OS) is the most common primary bone malignancy in children and young adults. MiR-205 has been reported to be negatively correlated with the proliferation and metastasis of many types of cancer, while its effects on the malignant phenotype of OS are unclear. Methods: Using TaqMan RT polymerase chain reaction analysis, we firstly explored the expression of miR-205 in a panel of OS cell lines. As the expression of miR-205 was significantly decreased in these cell lines, we sought to compensate for its loss by transfection of exogenous miR-205 mimic into MG-63 cells. To further understand the role of miR-205 in OS, we investigated the effects of miR-205 on the proliferation, migration, and invasion of MG-63 cells, and further explored the mechanisms that might be involved. Results: We found that miR-205 was consistently suppressed in OS cells when compared with the normal human osteoblast (NHOst) cell line. Restored expression of miR-205 in the OS (MG-63) cell line significantly inhibited cell proliferation, migration, and invasion. Moreover, bioinformatic prediction suggested that vascular endothelial growth factor A (VEGFA) was the target oncogene for miR-205 in OS cells. Further quantitative RT polymerase chain reaction and Western blot assays identified that overexpression of miR-205 suppressed expression of VEGFA mRNA and protein. Restored expression of VEGFA in MG-63 cells previously treated with miR-205 mimic could partially abolish miR-205-mediated suppression of proliferation and invasion of these cells. Conclusion: Collectively, these data suggest that miR-205 might function as a tumor suppressor in OS by, at least partially, targeting VEGFA. Keywords: miR-205, osteosarcoma, vascular endothelial growth factor A, metastasis