Suppression of scinderin modulates epithelial‑mesenchymal transition markers in highly metastatic gastric cancer cell line SGC‑7901.

Scinderin is a Ca2+‑dependent filamentous actin (F‑actin) severing and capping protein, which has a key role in regulated secretion. However, little is known regarding the function and mechanism of scinderin in human carcinoma development and progression. In the present study, the biological function of scinderin was investigated using a cell proliferation assay, flow cytometric analysis and a Transwell assay in highly tumorigenic and the metastatic human gastric cancer cell line SGC‑7901 transfected with scinderin‑small hairpin RNA lentivirus. The changes in the expression of epithelial‑mesenchymal transition (EMT) markers were also investigated. The results indicated that scinderin knockdown effectively suppressed proliferation, reduced migration and arrested the cell cycle of the SGC‑7901 cells at G2/M phase. Furthermore, scinderin knockdown altered the expression of EMT markers; the expression of E‑cadherin was significantly upregulated, along with an evident decrease in N‑cadherin and β‑catenin expression. In conclusion, the present study suggested that suppression of scinderin impaired proliferation and migration of gastric cancer SGC‑7901 cells and attenuates its EMT process. Scinderin may therefore be a potential target for tumor EMT and therapy against gastric cancer.