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 specific role of lncRNA MNX1-AS1 in the development of gastric cancer (GC), and to explore the underlying mechanism. PATIENTS AND METHODS: MNX1-AS1 expression in both GC cells and tissue samples was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the relationship between MNX1-AS1 expression and the overall survival rate of GC patients was explored. Furthermore, wound healing assay and transwell assay were conducted. In addition, the underlying mechanism of MNX1-AS1 in GC was explored by performing RT-qPCR and Western blot assay. RESULTS: MNX1-AS1 expression in GC samples was significantly higher than that of the corresponding normal tissues. Meanwhile, MNX1-AS1 expression was associated with the overall survival time of GC patient. Moreover, the migration and invasion of GC cells were markedly promoted after MNX1-AS1 overexpression in vitro. The mRNA and protein expressions of CDKN1A were remarkably down-regulated after MNX1-AS1 overexpression. Furthermore, the expression level of CDKN1A was negatively correlated with the expression of MNX1-AS1 in GC tissues. CONCLUSIONS: Our results suggested that MNX1-AS1 could enhance the metastasis and invasion of GC cells via suppressing CDKN1A. Furthermore, MNX1-AS1 might be a potential therapeutic target for GC.
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 specific role of lncRNA MNX1-AS1 in the development of gastric cancer (GC), and to explore the underlying mechanism. PATIENTS AND METHODS: MNX1-AS1 expression in both GC cells and tissue samples was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the relationship between MNX1-AS1 expression and the overall survival rate of GC patients was explored. Furthermore, wound healing assay and transwell assay were conducted. In addition, the underlying mechanism of MNX1-AS1 in GC was explored by performing RT-qPCR and Western blot assay. RESULTS:MNX1-AS1 expression in GC samples was significantly higher than that of the corresponding normal tissues. Meanwhile, MNX1-AS1 expression was associated with the overall survival time of GC patient. Moreover, the migration and invasion of GC cells were markedly promoted after MNX1-AS1 overexpression in vitro. The mRNA and protein expressions of CDKN1A were remarkably down-regulated after MNX1-AS1 overexpression. Furthermore, the expression level of CDKN1A was negatively correlated with the expression of MNX1-AS1 in GC tissues. CONCLUSIONS: Our results suggested that MNX1-AS1 could enhance the metastasis and invasion of GC cells via suppressing CDKN1A. Furthermore, MNX1-AS1 might be a potential therapeutic target for GC.