Inhibition of gastric cancer cell apoptosis by long noncoding RNA TRPM2‐AS via mitogen‐activated protein kinase and activators of transduction‐3

Background and Aim Long noncoding RNA TRPM2‐AS has emerged as a novel regulator in cancer initiation and progression of various cancers. However, the function and underlying mechanism of TRPM2‐AS in the progression of gastric cancer (GC) remain poorly understood. Methods GEO and TCGA databases were used for isolation of differential lncRNA expression. TRPM2‐AS expression levels in GC tissues and cells were measured by quantitative polymerase chain reaction method. TRPM2‐AS subcellular location was detected by fluorescence in situ hybridization analysis. The functional roles of TRPM2‐AS in cells were analyzed by loss and gain function assays. Results By using bioinformatics and quantitative polymerase chain reaction methods, TRPM2‐AS expression levels were proved to be upregulated in GSE70880 dataset, TCGA database, and 26 GC tissues, which was partly induced by SP1. The results of clinical assays showed that TRPM2‐AS could be an indicator for early‐stage GC diagnosis. Fluorescence in situ hybridization analysis showed that TRPM2‐AS was located in both nucleus and cytoplasm. Functional experiments displayed that knockdown of TRPM2‐AS inhibited proliferation, migration, and invasion in GC cells. Furthermore, depression of TRPM2‐AS suppressed cell growth though promotion of cell apoptosis. The expression levels of cleaved PARP, caspase 9, caspase 3, and Bax were significantly increased in BGC823 with TRPM2‐AS knockdown. In addition, knockdown of TRPM2‐AS reduced and phosphorylate signal transducer and activator of transcription 3 and increased and phosphorylate p38 mitogen‐activated protein kinase. Conclusions This study demonstrated that SP1‐regulated TRPM2‐AS is involved in GC cell apoptosis probably via p38 mitogen‐activated protein kinase and signal transducer and activator of transcription 3 pathways, indicating that TRPM2‐AS might be a potential therapeutic target in GC.