Résumé
Objective To study the effect of CKS2 on filopodia formation of A2780 cells through regulating CDC42 alternative splicing. Methods The filopodia were observed after CKS2 of A2780 cells were knocked down by lentivirus-mediated shRNA; the migrating ability of A2780 cells was also measured by wound healing assay; the expression levels of splicing variants CDC42-V1 and CDC42-V2 mRNA was determined by real time PCR after CKS2 knockdown. The expression levels of CKS2, CDC42-V1 and CDC42-V2 mRNA were further measured in each ovarian cancer and normal ovarian samples in the same way. Results The filopodia on A2780 cells obviously decreased, and the migrating ability of A2780 cells was also remarkably reduced after CKS2 knockdown (P<0.05). Meanwhile the expression of CDC42-V1 mRNA decreased and CDC42-V2 mRNA increased after CKS2 knockdown (P<0.05). Real time PCR results showed that the mRNA expression levels of CKS2 and CDC42-V1 were higher in ovarian cancer samples than in normal ovarian tissues; however, the expression level of CDC42-V2 mRNA was lower in ovarian cancer samples than in normal ovarian tissues (P<0.05). ConclusionCKS2 may affect the filopodia formation of A2780 cells through regulating CDC42 alternative splicing, and further affect the migrating ability of A2780 cells.