LncRNA mediates expression by targeting and affects the growth of gastric cancer.

Background: Long non-coding ribonucleic acids (lncRNAs) are a class of non-coding RNAs implicated in the development of many malignancies, including gastric cancer (GC). In this study, we investigated the functions and molecular mechanisms of non-coding RNA activated by deoxyribonucleic acid damage () in GC.

Methods: expression at the messenger RNA levels was determined by quantitative reverse transcriptase (RT)-polymerase chain reaction assays. Cell proliferation, migration, and invasion were detected by Cell Counting Kit-8 assays, tumor formation assays, and Transwell assays. Cell-cycle distribution was detected by a flow cytometry analysis. location was detected by nucleocytoplasmic fractionation assays. The interaction between and the ()/ () axis was verified by dual-luciferase reporter gene assays and RNA binding protein immunoprecipitation (RIP) assays. Western blot was used to study the phosphatase and tensin homolog ()/phosphoinositide 3-kinases ()/protein kinase B () signaling pathway.

Results: NORAD was upregulated in the GC tissues and cell lines. The silencing of repressed cell proliferation and the Growth 2 (G2)/Mitosis (M) cell-cycle transition in GC. also regulated expression by targeting and mediated signaling in GC.

Conclusions: We found that acts as an oncogene in GC. Our findings might provide a novel therapeutic target for GC.