MicroRNA-25 suppresses proliferation, migration, and invasion of osteosarcoma by targeting SOX4. Issue 7 (July 2017)

• Record Type: Journal Article
• Authors: Chen, Bingpeng; Liu, Jingjing; Qu, Ji; Song, Yang; Li, Yuxiang; Pan, Su
• Is Part Of: Tumor biology. Volume 39:Issue 7(2017)
• Publication Date: 2017-07
• Subjects: Osteosarcoma -- miR-25 -- SOX4 -- epithelial–mesenchymal transition; Cancer -- Periodicals; Oncology -- Periodicals; Tumors -- Periodicals; 616.994
• DOI: 10.1177/1010428317703841
• Languages: English
• ISSNs: 1010-4283

Abstract

Altered expression of the miR-25 has been implicated in many human malignant progression as oncogene or tumor suppressor. However, the precise role of miR-25 in osteosarcoma progression remains largely unclear. This study aimed to investigate the role and underlying mechanism of miR-25 in osteosarcoma. In this study, we demonstrated that miR-25 was significantly downregulated in osteosarcoma cell lines and tissues and that lower miR-25 was associated with advanced tumor–node–metastasis stage and lymph node metastasis. Then, we found that introduction of miR-25 significantly suppressed the proliferation, colony formation, migration, and invasion of osteosarcoma cells in vitro and retarded tumor growth in vivo. Further studies indicated that the epithelial–mesenchymal transition–related transcription factor, SOX4 (SRY-related high-mobility group box 4), was a direct target gene of miR-25, evidenced by bioinformatics analysis predicted and luciferase reporter assay. Furthermore, miR-25 could decrease the expression of SOX4 levels and inhibited epithelial–mesenchymal transition process. The levels of miR-25 were inversely correlated with those of SOX4 expression in osteosarcoma tissues. SOX4 overexpression rescued miR-25-induced suppression of proliferation, migration, and invasion of osteosarcoma cells. Taken together, these results suggest that miR-25 functions as a tumor suppressor in the progression of osteosarcoma by repressing SOX4.