Long non-coding RNA BCAR4 accelerates cell proliferation and suppresses cell apoptosis in gastric cancer via regulating MAPK/ERK signaling.

ABSTRACT

OBJECTIVE: As the fourth most common malignant tumor with high mortality rate, gastric cancer (GC) seriously threatens people's health and life quality worldwide. The aim of this study was to explore the functional role of long non-coding RNA (lncRNA) BCAR4 in GC. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was used to detect the expression level of lncRNA BCAR4 in GC cell lines and tissues. Subsequently, cell counting kit-8 (CCK-8) assay, colony formation assay, and flow cytometry were recruited to investigate the role of lncRNA BCAR4 in the proliferation and apoptosis of GC cells, respectively. Western blotting was used to detect the protein expression level of mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated kinase (ERK) in GC. Besides, tumor formation assay was applied to examine the ability of lncRNA BCAR4 in vivo. RESULTS: LncRNA BCAR4 was highly expressed in both GC tissues and cell lines. CCK-8 assay, colony formation assay, and flow cytometry results indicated that up-regulated lncRNA BCAR4 significantly promoted cell proliferation and suppressed cell apoptosis in GC. Besides, over-expression of lncRNA BCAR4 could activate the MAPK/ERK signaling pathways. Tumor xenograft formation assay demonstrated that over-expression of lncRNA BCAR4 promoted tumor formation in vivo. CONCLUSIONS: LncRNA BCAR4 was proved significantly up-regulated in GC. Over-expression of lncRNA BCAR4 promoted cell proliferation and suppressed cell apoptosis in vitro and promoted tumor formation in vivo. Besides, Western blotting revealed that lncRNA BCAR4 played an oncogenic role in GC via regulating MAPK/ERK signaling.