RPL35A is a key promotor involved in the development and progression of gastric cancer

Background RPL35A has been reported to work as a biomarker in tumor angiogenesis. However, little work has been performed on the expression level and functional importance of RPL35A in gastric cancer (GC). Methods The protein expression level of RPL35A was detected by immunohistochemical staining and western blot analysis. The Celigo cell counting assay was used to assess cell proliferation. Both the wound healing assay and the transwell assay were conducted to evaluate cell migration. Flow cytometric analysis was utilized to detect cell apoptosis and cell cycle. A mouse xenograft model was constructed for in vivo experiments. Results The results demonstrated that RPL35A expression was abundantly up-regulated in GC and positively related to tumor infiltrate. In addition, RPL35A knockdown could significantly suppress cell proliferation, migration, enhance apoptosis and arrest cell cycle. The in vivo study also verified the inhibitory effects of RPL35A knockdown on GC tumorigenesis. Conclusions The above mentioned results indicated that the knockdown of RPL35A might be a considerable therapeutic strategy for the treatment of gastric cancer.

Automated summary

RPL35A expression is highly up-regulated in gastric cancer and positively correlated with tumor infiltrate. Knockdown of RPL35A significantly inhibits cell proliferation, migration, enhances apoptosis, and arrests the cell cycle. In vivo experiments confirm the inhibitory effects of RPL35A knockdown on gastric cancer tumorigenesis.