Q You1, H-Y Shi, C-F Gong, X-Y Tian, S Li. 1. Department of Gynecology and Obstetrics, The First Affiliated Hospital of Harbin Medical University, Harbin, China. yqvicky2001@sina.com.
Abstract
OBJECTIVE: Recently, long non-coding RNAs (lncRNAs) have been extensively studied for their role in tumor progression. This work explored the role of lncRNA DLX6-AS1 in mediating the development of ovarian cancer (OC). PATIENTS AND METHODS: DLX6-AS1 expression was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) in OC tissues. Moreover, wound healing assay and transwell assay were performed to detect the effect of DLX6-AS1 on the metastasis of OC. Furthermore, the underlying mechanism of DLX6-AS1 in mediating the progression of OC was explored through the Dual-Luciferase reporter gene assay and RNA immunoprecipitation assay (RIP). RESULTS: DLX6-AS1 expression was higher in OC samples than that in the adjacent ones. Moreover, cell migration and invasion were suppressed after DLX6-AS1 knockdown in vitro. Conversely, cell migration and invasion were promoted by overexpressed DLX6-AS1. Moreover, the expression of microRNA-613 (miR-613) was upregulated via knockdown of DLX6-AS1, but was downregulated after overexpression of DLX6-AS1. Furthermore, the Luciferase reporter gene assay and RIP assay showed that miR-613 was a direct target of MIAT in DLX6-AS1 in OC tissues. CONCLUSIONS: DLX6-AS1 could enhance migration and invasion of OC cells via targeting miR-613, which might serve as a potential therapeutic target in OC.
OBJECTIVE: Recently, long non-coding RNAs (lncRNAs) have been extensively studied for their role in tumor progression. This work explored the role of lncRNA DLX6-AS1 in mediating the development of ovarian cancer (OC). PATIENTS AND METHODS: DLX6-AS1 expression was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) in OC tissues. Moreover, wound healing assay and transwell assay were performed to detect the effect of DLX6-AS1 on the metastasis of OC. Furthermore, the underlying mechanism of DLX6-AS1 in mediating the progression of OC was explored through the Dual-Luciferase reporter gene assay and RNA immunoprecipitation assay (RIP). RESULTS:DLX6-AS1 expression was higher in OC samples than that in the adjacent ones. Moreover, cell migration and invasion were suppressed after DLX6-AS1 knockdown in vitro. Conversely, cell migration and invasion were promoted by overexpressed DLX6-AS1. Moreover, the expression of microRNA-613 (miR-613) was upregulated via knockdown of DLX6-AS1, but was downregulated after overexpression of DLX6-AS1. Furthermore, the Luciferase reporter gene assay and RIP assay showed that miR-613 was a direct target of MIAT in DLX6-AS1 in OC tissues. CONCLUSIONS:DLX6-AS1 could enhance migration and invasion of OC cells via targeting miR-613, which might serve as a potential therapeutic target in OC.