Abstract
Background: To analyse how Semaphorin 6D (SEMA6D) expression and extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signal pathways are activated and how they influence gastric cancer proliferation, migration, and invasion. Methodology: SEMA6D expression was knocked down in human gastric cancer cells using RNA interference technology. In vitro assays were used to analyse how SEMA6D knockdown affects clone formation, migration, and invasion. ERK and PI3K/ AKT/mTOR signaling pathway related proteins were detected by immunoblotting. Results: In the si-NC group, Sema6D protein levels were higher than those in the si-1 and si-2 groups after knockdown of Sema6D, while in the si-1 group, Sema6D protein levels were higher than those in the si-2 group (P<0.05). P-PI3K, ERK/p-ERK, AKT/p-AKT, and mTOR/p-mTOR levels in the si-NC group were significantly higher than those in the si-1 and si-2 groups after knockdown of Sema6D (P < 0.05). It was found that scratch healing rate of SGC-7901 cells in si-NC group was higher than that in si-1 and si-2 groups, and the difference was statistically significant (P < 0.05). Conclusion: SEMA6D expression level can affect the biological behavior of gastric cancer cells. Keywords: Gastric cancer; extracellular signal-regulated kinase; semaphorin 6D; ERK and PI3K/AKT/mTOR; cell proliferation.
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