Overexpression of long non‐coding RNA RP11‐363E7.4 inhibits proliferation and invasion in gastric cancer

LncRNA RP11‐363E7.4 has been shown to be downregulated in gastric cancer (GC), while the effect of lncRNA RP11‐363E7.4 on GC and its potential molecular mechanisms is unclear. The purpose of this study was to explore the functional role and underlying molecular mechanisms of lncRNA RP11‐363E7.4 involved in GC progress.To address the question, quantitative real‐time PCR assay was performed to confirm lncRNA RP11‐363E7.4 expression levels in GC tissues and cell lines. Cell proliferation, apoptosis, migration and invasion were estimated using Cell Counting Kit‐8, colony formation, scratch wound healing and Transwell assays. Potential molecular mechanisms were evaluated using western blot assay. The results showed that lncRNA RP11‐363E7.4 was significantly downregulated in GC cell lines and 82 paired tissues. The correlation between expression and clinicopathological features indicated that low expression of lncRNA RP11‐363E7.4 was associated with T stage (P = .010). Functional experiments showed that overexpression of lncRNA RP11‐363E7.4 prevented proliferation, migration, and invasion and induced apoptosis of GC cells. Western blot assay revealed that lncRNA RP11‐363E7.4 functioned via the p53, Bax/Bcl‐2, β‐catenin pathway. In summary, this study revealed that lncRNA RP11‐363E7.4 functioned as a tumour suppressor by inhibiting proliferation, migration, and invasion and inducing apoptosis of GC cells. Significance of the study:LncRNA RP11‐363E7.4 has been shown to be downregulated in GC, while the effect of lncRNA RP11‐363E7.4 on GC and its potential molecular mechanism is unclear. We revealed that lncRNA RP11‐363E7.4 functioned as a tumour suppressor by inhibiting proliferation, migration, and invasion and inducing apoptosis of GC cells. LncRNA RP11‐363E7.4 might become an attractive diagnostic and prognostic biomarker of GC and a promising target for GC treatment.