C-W Liu1, D Liu, D Peng. 1. Department of Orthopaedic Surgery, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China. pengdan_med@126.com.
Abstract
OBJECTIVE: Zinc finger antisense 1 (ZFAS1), a newly identified lncRNA, is aberrantly regulated in various cancers including osteosarcoma (OS). However, the underlying molecular mechanisms of ZFAS1 in OS remain to be elucidated. MATERIALS AND METHODS: We used transfection, luciferase report assay, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), colony formation assay, transwell migration, invasion assays, and Western blot to determine the potential mechanisms. RESULTS: Our study showed that ZFAS1 was up-regulated in OS cells and promoted the colony formation, migration, and invasion of OS cells via activating the MAPK signaling pathway. Furthermore, the experimental results indicated that miR-646 was a target of ZFAS1 and there was a negative relationship between ZFAS1 and miR-646 expression. Additionally, we found that ZFAS1 in OS cells up-regulated the expression of NOB1 through sponging miR-646, finally facilitating the growth of the OS cells. CONCLUSIONS: These results demonstrated that ZFAS1/miR-646/NOB1 axis might play an important role in the development of OS, and ZFAS1 and miR-646 can be considered as potential biomarkers for the diagnosis and treatment of OS.
OBJECTIVE:Zinc finger antisense 1 (ZFAS1), a newly identified lncRNA, is aberrantly regulated in various cancers including osteosarcoma (OS). However, the underlying molecular mechanisms of ZFAS1 in OS remain to be elucidated. MATERIALS AND METHODS: We used transfection, luciferase report assay, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), colony formation assay, transwell migration, invasion assays, and Western blot to determine the potential mechanisms. RESULTS: Our study showed that ZFAS1 was up-regulated in OS cells and promoted the colony formation, migration, and invasion of OS cells via activating the MAPK signaling pathway. Furthermore, the experimental results indicated that miR-646 was a target of ZFAS1 and there was a negative relationship between ZFAS1 and miR-646 expression. Additionally, we found that ZFAS1 in OS cells up-regulated the expression of NOB1 through sponging miR-646, finally facilitating the growth of the OS cells. CONCLUSIONS: These results demonstrated that ZFAS1/miR-646/NOB1 axis might play an important role in the development of OS, and ZFAS1 and miR-646 can be considered as potential biomarkers for the diagnosis and treatment of OS.