D-W Zhang1, G-Q Gu, X-Y Chen, G-C Zha, Z Yuan, Y Wu. 1. Department of Orthopedics, The Affiliated Shuyang Hospital of Xuzhou Medical University, Jiangsu, China. yongwu@ashxmu.com.
Abstract
OBJECTIVE: Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis and development of multiple cancers, including osteosarcoma (OS). The present study aims to investigate the role of LINC00665 in OS progression. PATIENTS AND METHODS: The expression levels of LINC00665 and miR-3619 were assessed by RT-qPCR. The correlation between LINC00665 and miR-3619 expression was evaluated by Pearson's correlation analysis. The interaction between LINC00665 and miR-3619 was predicted by starBase, which was further confirmed by Luciferase reporter assay and RIP assay. The viability, invasion, and migration of OS cells were analyzed by CCK-8 and transwell assays. RESULTS: LINC00665 expression was upregulated in OS tissues and cell lines, and the high level of LINC00665 was associated with poor prognosis in OS. Moreover, LINC00665 knockdown attenuated the viability, invasion, and migration of OS cells. In addition, miR-3619 was demonstrated to be a target of LINC00665. Overexpression of miR-3619 inhibited OS progression, while this effect was abolished by the upregulation of LINC00665. CONCLUSIONS: We demonstrated that LINC 00665 accelerated OS development by targeting miR-3619. These findings might provide potential treatment strategies for patients with OS.
OBJECTIVE: Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis and development of multiple cancers, including osteosarcoma (OS). The present study aims to investigate the role of LINC00665 in OS progression. PATIENTS AND METHODS: The expression levels of LINC00665 and miR-3619 were assessed by RT-qPCR. The correlation between LINC00665 and miR-3619 expression was evaluated by Pearson's correlation analysis. The interaction between LINC00665 and miR-3619 was predicted by starBase, which was further confirmed by Luciferase reporter assay and RIP assay. The viability, invasion, and migration of OS cells were analyzed by CCK-8 and transwell assays. RESULTS:LINC00665 expression was upregulated in OS tissues and cell lines, and the high level of LINC00665 was associated with poor prognosis in OS. Moreover, LINC00665 knockdown attenuated the viability, invasion, and migration of OS cells. In addition, miR-3619 was demonstrated to be a target of LINC00665. Overexpression of miR-3619 inhibited OS progression, while this effect was abolished by the upregulation of LINC00665. CONCLUSIONS: We demonstrated that LINC 00665 accelerated OS development by targeting miR-3619. These findings might provide potential treatment strategies for patients with OS.