OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) play essential roles in tumorigenesis. The aim of this study was to investigate the exact role of lncRNA DLX6-AS1 in the development of colorectal cancer (CRC), and to explore the possible mechanism. PATIENTS AND METHODS: DLX6-AS1 expression in CRC tissues was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Function assays were conducted to detect the effect of DLX6-AS1 on the proliferation and metastasis of CRC in vitro. Furthermore, luciferase reporter gene assay and RNA immunoprecipitation assay (RIP) were used to explore the underlying mechanism of DLX6-AS1. RESULTS: DLX6-AS1 expression in CRC samples was significantly higher than that of adjacent tissues. Loss of DLX6-AS1 markedly inhibited the proliferation, migration, and invasion of CRC cells. Furthermore, luciferase reporter gene assay and RIP assay showed that DLX6-AS1 acted as a competing endogenous RNA via sponging miR-577 in CRC. CONCLUSIONS: DLX6-AS1 could promote the proliferation, migration, and invasion of CRC by sponging miR-577, which might offer a potential therapeutic target for CRC.
OBJECTIVE: Recent researches have proved that long noncoding RNAs (lncRNAs) play essential roles in tumorigenesis. The aim of this study was to investigate the exact role of lncRNA DLX6-AS1 in the development of colorectal cancer (CRC), and to explore the possible mechanism. PATIENTS AND METHODS: DLX6-AS1 expression in CRC tissues was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Function assays were conducted to detect the effect of DLX6-AS1 on the proliferation and metastasis of CRC in vitro. Furthermore, luciferase reporter gene assay and RNA immunoprecipitation assay (RIP) were used to explore the underlying mechanism of DLX6-AS1. RESULTS:DLX6-AS1 expression in CRC samples was significantly higher than that of adjacent tissues. Loss of DLX6-AS1 markedly inhibited the proliferation, migration, and invasion of CRC cells. Furthermore, luciferase reporter gene assay and RIP assay showed that DLX6-AS1 acted as a competing endogenous RNA via sponging miR-577 in CRC. CONCLUSIONS:DLX6-AS1 could promote the proliferation, migration, and invasion of CRC by sponging miR-577, which might offer a potential therapeutic target for CRC.