RPS15a Silencing Suppresses Cell Proliferation and Migration of Gastric Cancer
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Purpose: Information on the possible role of the ribosomal protein S15a (RPS15a) in gastric cancer is scarce. The aim of this studywas to evaluate the impact of RPS15a gene expression on the growth and cell cycle of gastric cancer cells in vitro and in vivo. Materials and Methods: RPS15a mRNA expression was examined in cancer tissues and their corresponding adjacent normal tissuesof 40 gastric adenocarcinoma patients. Next, RPS15a was knocked down using a lentivirus-mediated RNA interference (shorthairpin RNA) system in the gastric cancer cell line BGC823. The effect of RPS15a knockdown was examined using CCK-8 assay,cell scratch test, colony formation assay, and flow cytometry. Finally, in nude mice, a tumorigenicity test was performed, and thetumor volume and weight were measured. Results: RPS15a expression in tumor tissue was significantly greater than that in the adjacent normal tissue of gastric cancer patients. After RPS15a silencing, the BGC823 cell proliferation rate decreased significantly; most cells were arrested in the G0/G1phase, cell growth was inhibited, and the migration rate was decreased. Colony formation assay showed that the number and sizeof clones in the RPS15a-silenced cells were fewer and smaller, compared to control cells. The nude mouse tumorigenicity testshowed that RPS15a silencing had an inhibitory effect on tumor volume and mice weight. Conclusion: The present study found RPS15a expression to be higher in gastric tumors and its silencing in gastric cancer cells toinhibit the proliferation, growth, and migration thereof. Accordingly, RPS15a may be considered as a potential therapeutic targetin gastric cancer.
Abstract
Purpose: Information on the possible role of the ribosomal protein S15a (RPS15a) in gastric cancer is scarce. The aim of this studywas to evaluate the impact of RPS15a gene expression on the growth and cell cycle of gastric cancer cells in vitro and in vivo. Materials and Methods: RPS15a mRNA expression was examined in cancer tissues and their corresponding adjacent normal tissuesof 40 gastric adenocarcinoma patients. Next, RPS15a was knocked down using a lentivirus-mediated RNA interference (shorthairpin RNA) system in the gastric cancer cell line BGC823. The effect of RPS15a knockdown was examined using CCK-8 assay,cell scratch test, colony formation assay, and flow cytometry. Finally, in nude mice, a tumorigenicity test was performed, and thetumor volume and weight were measured. Results: RPS15a expression in tumor tissue was significantly greater than that in the adjacent normal tissue of gastric cancer patients. After RPS15a silencing, the BGC823 cell proliferation rate decreased significantly; most cells were arrested in the G0/G1phase, cell growth was inhibited, and the migration rate was decreased. Colony formation assay showed that the number and sizeof clones in the RPS15a-silenced cells were fewer and smaller, compared to control cells. The nude mouse tumorigenicity testshowed that RPS15a silencing had an inhibitory effect on tumor volume and mice weight. Conclusion: The present study found RPS15a expression to be higher in gastric tumors and its silencing in gastric cancer cells toinhibit the proliferation, growth, and migration thereof. Accordingly, RPS15a may be considered as a potential therapeutic targetin gastric cancer.
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