<p>Upregulated RACK1 attenuates gastric cancer cell growth and epithelial–mesenchymal transition via suppressing Wnt/β-catenin signaling</p>

Purpose: As there have been few studies on the effects of the receptor for activated C kinase 1 (RACK1) on gastric cancer (GC), we aimed to explore such effects and the mechanism that may be involved. Patients and methods: Normal gastric epithelial cells and six GC cell lines were used to detect the mRNA expression of RACK1. Overexpressing RACK1 was transfected in HGC27 and MGC803 cells. The effects of overexpressing RACK1 on cell viability, migration, and invasion were determined by cell counting kit-8, wound scratch, and Transwell assay, respectively. The expressions of epithelial–mesenchymal transition (EMT) and Wnt/β-catenin signaling related genes were detected using quantitative real-time PCR or Western blot. Wnt pathway agonist LiCl was added into RACK1 overexpressing GC cells, and then cell viability, migration, and invasion were also detected. Results: RACK1 was downregulated in GC cell lines. Under the circumstance that overexpressing RACK1 was successfully transfected in the two lowest RACK1-expressing GC cells, significant inhibition of cell viability, migration, and invasion, promotion to the mRNA and protein expression of E-cadherin, as well as a decrease in the N-cadherin and Snail expressions could be observed. Overexpressing RACK1 also enhanced the protein level of phosphorylation-β-catenin/β-catenin and attenuated c-Jun protein expression. Additionally, LiCl could partially reverse the inhibitory effects of cell viability, migration and invasion by overexpressing RACK. Conclusion: We found RACK1 possibly inhibited epithelial–mesenchymal transition of GC cells through limitation of the Wnt/β-catenin pathway, thereby suppressing cell migration and invasion; RACK1 could also suppress cell growth. Keywords: RACK1, gastric cancer, LiCl, Wnt/β-catenin signaling, epithelial-mesenchymal transition