Effects of shRNA targeting PRL-3 on proliferation,invasion and apoptosis of human colorectal cancer cells

WANG Yan; ZHANG Jiao; WANG Hui-feng; WANG Ning-ju

doi:10.11958/20171068

Abstract：Objective To investigate the effects of PRL-3 shRNA mediated by lentivirus on proliferation, invasion and apoptosis of human colorectal cancer SW480 cells. Methods There were three experimental groups in this study, which included blank control group, negative control group and transfected group. Colorectal cancer SW480 cells were transfected with lentiviral interference vector carrying PRL-3 shRNA to build a stable PRL-3-silencing cell line. The expression of PRL-3 mRNA was detected by real-time quantitative polymerase chain reaction (real-time PCR). Cell proliferation was analyzed by MTT method and colony formation assay.Invasion and migration were measured by Transwell assay and invasion chamber. Apoptosis rate was performed by flow cytometry. Results The stable PRL-3-silencing cell line was successfully constructed.Compared with the blank control group and negative control group,the relative expression levels of PRL-3 mRNA were reduced in transfected group after transfection with PRL-3 shRNA(P<0.05),but there was no significant difference between the blank control group and the negative control group.After transfection with PRL-3 shRNA for 72 h,the proliferation of SW480 cells was significantly lower in transfected group than that of the blank control group and the negative control group,and the proliferation decreased significantly in 120 h(P<0.05).Compared with the blank control group and negative control group, the ability of colony formation was also weakened in the transfected group (P<0.05). Compared with the blank control group and negative control group,the migration and invasion ability were decreased in the transfected group(P<0.05),and the apoptosis rate was increased in the transfected group(P<0.05).Conclusion PRL-3 shRNA can inhibit the expression of PRL-3 and the proliferation, promote the apoptosis of SW480, which indicates that PRL-3 may become a target for colorectal carcinoma treatment.