AKAP12 inhibits the proliferation of ovarian cancer by activating the Hippo pathway

Abstract

Abstract Background Ovarian cancer is a prominent cause of mortality among women worldwide. A kinase anchor protein 12 (AKAP12) has been investigated, but its contribution to ovarian cancer is unclear. Objectives This study comprehensively investigates the role of AKAP12 in ovarian cancer proliferation by elucidating its underlying mechanisms and functions. Methods We compared the expression levels of AKAP12 in ovarian cancer and adjacent tissues. We subsequently established A2780 and HO8910 cell lines that have undergone AKAP12 overexpression or knockdown to verify the function of AKAP12 in ovarian cancer. To determine the effect of AKAP12 on tumorigenicity, migration, and invasion, we performed CCK-8, colony-formation, xenograft models, transwell, and wound healing assays. Furthermore, we used pathway enrichment analysis to identify Hippo signaling related to AKAP12 overexpression. Then we characterized the relevance of Hippo signaling in AKAP12-regulated tumor suppressive effects in ovarian cancer through western blot. Results Our study revealed a significant decrease in AKAP12 expression in ovarian cancer samples. Moreover, functional assays demonstrated the tumor suppressive effects of AKAP12 overexpression, inhibiting cancer cell proliferation, migration, and invasion. Consistent with these findings, mice inoculated with AKAP12-overexpressing cells exhibited slower tumor growth in our mouse xenograft model. We also observed a positive relationship between AKAP12 overexpression and Hippo pathway-related proteins. Conclusions AKAP12 plays a crucial role in the suppression of ovarian cancer through activation of the Hippo signaling pathway. Furthermore, it could be a potential target for developing new therapeutic strategies for ovarian cancer treatment.