Objective  To investigate the effects of SMRACAD1 on gastric cancer cell proliferation and invasion and its mechanism.

Methods  Differential analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis of SMRACAD1 expression from 373 gastric cancer tissues and 32 normal tissues in The Cancer Genome Atlas (TCGA) database were performed; SMRACAD1 expression in human normal gastric mucosal epithelial cells (GES-1), human gastric cancer cells (HGC-27) and human gastric adenocarcinoma cells (AGS) was detected by protein blotting (Western blot, WB) and quantitative real-time polymerase chain reaction (qPCR). The model of down-regulated SMRACAD1 expression by AGS cells and a blank control model were constructed. The down-regulated SMRACAD1 expression and blank control model of AGS cells were constructed, and the proliferation ability of AGS cells was detected by plate cloning and CCK-8 assay, the migration ability was detected by scratch assay, and the migration and invasion ability were detected by Transwell assay. The effects of SMRACAD1 down-regulation on the expression of epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin, N-cadherin, Vimentin, Snail) and PI3K/AKT/mTOR signaling pathways were detected by WB.

Results  SMRACAD1 was highly expressed in gastric cancer tissues and AGS cells. Down-regulating the SMRACAD1 expression inhibited the proliferation, invasion and migration ability of AGS cells (P<0.05), and inhibited the activation of EMT process and PI3K/AKT/mTOR signaling pathways in AGS cells.

Conclusion  SMARCDA1 is upregulated in gastric cancer tissues and cell lines, and the downregulation of SMRACAD1 expression by inhibiting activation of the PI3K/AKT/mTOR signaling pathways can inhibit gastric cancer cell proliferation, invasion, migration, and EMT.

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