Upregulation of FTX Promotes Osteosarcoma Tumorigenesis by Increasing SOX4 Expression via miR-214-5p

BACKGROUND: Long-chain non-coding RNA (LncRNA) plays a key role in the biological processes of tumors. LncRNA-FTX has been the invasion of tumors. However, its function and mechanism in osteosarcoma have not been studied. METHODS: qRT-PCR was measured the expression levels of FTX and miR-214-5p in osteosarcoma. The protein levels of SRY-related HMG box transcription factor 4 (SOX4) were detected by Western Blot. Cholecystokinin (CCK-8) assay, cell colony formation and Transwell assay, Annexin V-FITC/PI assay were analyzed the effects of FTX and miR-214-5p on cell proliferation, cell invasion and apoptosis. The relationship between FTX, miR-214-5p and SOX4 was analyzed by bioinformatics analysis and Luciferase. The tumor changes in mice were detected by vivo experiments in nude mice. RESULTS: The expression levels of FTX were increased in osteosarcoma tissues and cell lines and negatively correlated with the expression levels of miR-214-5p. FTX could modulate the expression of miR-214-5p in osteosarcoma cell lines. sh-FTX inhibited the growth and metastasis of osteosarcoma. FTX could regulate the growth of osteosarcoma through miR-214-5p. The knockdown of miR-214-5p reversed the inhibitory effect of sh-FTX on osteosarcoma cell proliferation and growth in mice. Furthermore, FTX regulated the expression of SOX4 by acting as a sponge of miR-214-5p in osteosarcoma. CONCLUSION: FTX could promote proliferation, invasion and inhibited apoptosis by regulating miR-214-5p/SOX4 axis in osteosarcoma, suggesting that FTX might be a potential target for osteosarcoma treatment.