OBJECTIVE: Recently, long non- coding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in the development of thyroid cancer (TC), and to explore the underlying mechanism. PATIENTS AND METHODS: DLX6-AS1 expression in both TC cells and tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, transwell assay and wound healing assay were conducted. QRT-PCR and Western blot assay were used to explore the underlying mechanism. Furthermore, the function of DLX6-AS1 was identified in vivo. RESULTS: DLX6-AS1 expression level in TC tissues was significantly higher than that of the corresponding normal tissues. Moreover, TC cell migration and invasion were markedly inhibited after DLX6-AS1 was knocked down in vitro. The mRNA and protein expressions of UPF1 were both remarkably up-regulated after knockdown of DLX6-AS1. Meanwhile, the expression level of UPF1 was negatively correlated with the expression of DLX6-AS1 in TC tissues. Furthermore, knockdown of DLX6-AS1 significantly inhibited tumor metastasis in vivo. CONCLUSIONS: Knockdown of DLX6-AS1 could inhibit TC cell migration and invasion via upregulating UPF1, which might be a potential therapeutic target in TC.
OBJECTIVE: Recently, long non- coding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) in the development of thyroid cancer (TC), and to explore the underlying mechanism. PATIENTS AND METHODS: DLX6-AS1 expression in both TC cells and tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, transwell assay and wound healing assay were conducted. QRT-PCR and Western blot assay were used to explore the underlying mechanism. Furthermore, the function of DLX6-AS1 was identified in vivo. RESULTS:DLX6-AS1 expression level in TC tissues was significantly higher than that of the corresponding normal tissues. Moreover, TC cell migration and invasion were markedly inhibited after DLX6-AS1 was knocked down in vitro. The mRNA and protein expressions of UPF1 were both remarkably up-regulated after knockdown of DLX6-AS1. Meanwhile, the expression level of UPF1 was negatively correlated with the expression of DLX6-AS1 in TC tissues. Furthermore, knockdown of DLX6-AS1 significantly inhibited tumor metastasis in vivo. CONCLUSIONS: Knockdown of DLX6-AS1 could inhibit TC cell migration and invasion via upregulating UPF1, which might be a potential therapeutic target in TC.