Abstract
Long non-coding RNAs (lncRNAs) are crucial for gastric cancer (GC) progression. In this study, we aimed to investigate the function and molecular pathways of lncRNA C2orf27A in GC development. Bioinformatics databases, tissue cDNA microarrays, and cell lines were used to assess the expression of C2orf27A in GC. Cell proliferation was assessed using Cell Counting Kit-8, colony formation, cell cycle assays, whereas cell death using the Annexin V-APC/7-AAD assay. Subcutaneous xenograft mouse models were used to assess the effects of the C2orf27A knockdown on GC growth in vivo. The subcellular localization of C2orf27A in GC cells was verified using nucleocytoplasmic separation. Bioinformatics analysis predicted the binding of C2orf27A, miR-610, and NADPH oxidase 4 (NOX4), which was validated using dual luciferase reporter gene assay. We found that C2orf27A expression increased in GC tissues and cells. Furthermore, GC patients with increased C2orf27A expression levels had worse survival rates. Silencing of C2orf27A suppressed GC cell growth and induced GC cell death in vitro and in vivo. Further investigations into underlying mechanisms showed that C2orf27A functions as a competitive endogenous RNA against miR-610, leading to increased NOX4 expression levels in GC cells. Notably, blocking miR-610 and increasing NOX4 expression levels reversed the anticancer effects of reduced C2orf27A levels in GC cells. In summary, C2orf27A promotes cell proliferation and reduces cell death through the miR-610/NOX4 pathway in GC, which may provide a new perspective for further elucidation of the molecular mechanism underlying GC progression.