Upregulation of long non-coding RNA DQ786243 promotes the progression of gastric cancer.

Long non‑coding RNAs (lncRNAs) have been identified as key regulatory factors in various biological processes. Their dysregulation has been observed in several types of human cancer, including gastric cancer (GC). The aim of the present study was to investigate the putative roles of the lncRNA DQ786243 in the progression of GC, as well as evaluate its diagnostic and therapeutic potential in GC. The expression of DQ786243 in 82 pairs of GC tissues and adjacent healthy tissues, as well as in three GC cell lines and a human normal gastric epithelial cell line, was assessed using reverse transcription‑quantitative polymerase chain reaction. In addition, the putative correlation between the expression of DQ786243 and various clinicopathological features of GC was investigated. Furthermore, the effects of silencing DQ786243 in GC cells were examined using RNA interference. Colony formation and Cell Counting kit‑8 assays were used to evaluate the effects of DQ786243 on GC cell proliferation, and Transwell and wound healing assays were used to examine GC cell migration and invasion. The results of the present study demonstrated that the expression of DQ786243 was significantly upregulated in GC tissues and cell lines compared with healthy control tissues and cells. Correlation analysis revealed a significant association between the expression of DQ786243 and the TNM stage, tumor size, depth of invasion and presence of lymph node metastasis in patients with GC. Furthermore, silencing the DQ786243 was demonstrated to inhibit proliferation, and impair the migration and invasion of GC cells. The present results suggested that DQ786243 may function as an oncogenic regulator via promoting the proliferation and metastasis of GC cells. Therefore, DQ786243 may have potential as a novel biomarker for the diagnosis of GC, and may also be a promising candidate for the development of novel therapeutic approaches for the treatment of patients with GC.