Long Non-Coding Rna Rp1-163g9.1 Is Downregulated In Gastric Adenocarcinoma And Is Associated With A Poor Prognosis

The aim of the present study was to investigate the expression, function and underlying molecular mechanism of the long non-coding (lnc) RNA RP1-163G9.1 in patients with gastric adenocarcinoma (GA). The expression levels of lncRNA RP1-163G9.1 were determined in 112 paired clinical GA tissues by reverse transcription-quantitative polymerase chain reaction analysis. Subsequently, the potential clinical values of lncRNA RP1-163G9.1 were analyzed with statistical methods. Additionally, the function of lncRNA RP1-163G9.1 was explored at the cellular level using the Cell Counting Kit-8 proliferation assay, Transwell experiments, fluorescence in situ hybridization (FISH), colony formation assay and flow cytometry. Furthermore, the function of lncRNA RP1-163G9.1 was assessed in vivo using subcutaneous tumorigenesis experiments in nude mice. lncRNA RP1-163G9.1 expression in GA tissues and cells was significantly decreased when compared with that in control gastric tissues (P<0.001) or gastric epithelial cells GES-1 (P<0.05). This finding was associated with the depth of invasion (P=0.001), lymph node metastasis (P=0.009), tumor size (P=0.037) and immunocytochemistry marker Ki-67 (P=0.010). FISH detection demonstrated that lncRNA RP1-163G9.1 was primarily located in the cytoplasm. Notably, overexpression of lncRNA RP1-163G9.1 significantly decreased cell proliferation (P<0.01), colony formation (P<0.01), invasion (P<0.01) and the number of cells at the S-phase of the cell cycle (P<0.05); However, it did not exert a significant effect on apoptosis (P>0.05). Furthermore, tumor formation experiments revealed that overexpression of lncRNA RP1-163G9.1 inhibited cancer cell proliferation in nude mice. The present research indicated that low expression of lncRNA RP1-163G9.1 may be associated with enhanced tumor proliferation and invasion in GA.