Elevated MYO10 Predicts Poor Prognosis and its Deletion HampersProliferation and Migration Potentials of Cells Through Rewiring PI3K/AktSignaling in Cervical Cancer

摘要

MYO10, recognized as an important regulator of cytoskeleton remodeling, has beenreported to be associated with tumorigenesis. However, its functionalimplication in cervical cancer and potential mechanism still remain to beundetermined currently. MYO10 level in cervical cancer tissues was analyzed byusing data retrieved from The Cancer Genome Atlas and ONCOMINE databases.Messenger RNA and protein expression levels were determined by quantitativereal-time polymerase chain reaction and Western blotting. Small-interfering RNAand overexpressing plasmid were used for MYO10 silencing and overexpression, andcell proliferation was analyzed by CCK-8. Transwell assays were performed toinvestigate the ability of cell migration and invasion. MYO10 was upregulated incervical cancer tissues and cells when compared to normal controls, and survivalanalysis showed patients with high MYO10 expression had worse overall survival.Moreover, knockdown/overexpression of MYO10 significantly inhibited/enhanced theproliferation, invasion, and migration capabilities of cervical cellstransfected with siRNAs/overexpressing plasmid. Additionally, MYO10 silencinginhibited PI3K/Akt signaling pathway by decreasing the phosphorylation status ofPI3K and AKT. Data from the present study indicated that MYO10 wereoverexpressed in patients with cervical cancer and positively linked with poorprognosis. Experimental results suggested that MYO10 induced a significantencouraging effect in cervical cancer cell proliferation, invasion, andmigration, linked with involvement of PI3K/Akt signaling. Collectively, theseresults emphasize a novel role for MYO10 overexpression in cervical cancer andprovide a potent therapeutic strategy against cervical cancer.