Background and purpose: LASP1 is a novel actin-binding protein and involved in the process of cytoskeleton reorganization and cell migration. Expression of LASP1 is significantly up-regulated in several malignant tumors and is closely related to the tumor proliferation

invasion and metastasis. However

the specific mechanism of LASP1 is not clear in gastric carcinogenesis. This study aimed to detect the effect and mechanism of LASP1 in the proliferation and invasion of gastric cancer cells. Methods: Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot were employed to determine the expression of LASP1 in gastric cancer cell lines

as well as human normal gastric epithelial cell line GES-1. RNA interference (RNAi) was used to silence the expression of LASP1 in gastric cancer cell BGC823. RTFQ-PCR and Western blot were used to analyze the expression of LASP1 after siRNA transfection. In vitro proliferation

migration and invasion assay were performed to detect the effect of LASP1 on BGC823 cells. F-actin polymerization assay was used to detect F-actin recognition ability in cells. Western blot was used to analyze phosphorylation of Akt. Results: Overexpression of LASP1 was detected in human gastric cancer BGC823 cells. Down-regulated expression of LASP1 at both mRNA and protein level was detected after siRNA transfection. Cell proliferation assay showed that the growth rate was significantly reduced in RNAi group (P0.05). In transwell assay

the cell migration and invasion were significantly decreased (P0.05). F-actin content was reduced compared with the control group (P0.05). The phosphorylation of Akt was significantly reduced after siRNA transfection. Conclusion: LASP1 was highly expressed in gastric cancer cells. Down-regulation of LASP1 suppressed the capacities of proliferation

migration and invasion of human gastric cancer BGC823 cells in vitro. LASP1 can induce migration and invasion of gastric cancer through regulation of F-actin polymerization and Akt phosphorylation.