Role of Semaphorin 3D in Inhibition of Colorectal Cancer Cell Migration by Regulating Actin Filament Associated Protein 1 Like 1

The abnormal expression of semaphorin 3D is associated with various tumors. Nevertheless, the function and mechanism in colorectal cancer have not been fully understood. This study aims at exploring the migration pattern and related mechanisms of semaphorin 3D in colorectal cancer cells in vitro. Human SW480 colorectal cancer cells lines were used in this study. Semaphorin 3D lentiviral overexpressed vector and control lentiviral vector were used to transfect SW480 cells. Quantification of semaphorin 3D, actin filament associated protein 1 like 1 messenger ribonucleic acid and protein levels were done by real-time quantitative polymerase chain reaction and western blotting. Ribonucleic acid sequencing is used for analysis of differential gene expression and transwell assay for determination of migration capacity. The research results showed that semaphorin 3D gene expression was dramatically overexpressed in SW480 cells that were transfected by semaphorin 3D lentiviral overexpressed vector. Compared to control group, cell migration capacity of semaphorin 3D overexpression SW480 cells were strikingly reduced. Ribonucleic acid sequencing, quantitative polymerase chain reaction and western blotting assays hinted actin filament associated protein 1 like 1 was significantly downregulated in semaphorin 3D overexpression cells. Based on these findings, overexpression of semaphorin 3D might prevent migration of colorectal cancer cells via down regulating actin filament associated protein 1 like 1. Therefore, semaphorin 3D may inhibit colorectal cancer cell migration and suppress colorectal cancer carcinogenesis and progression.