ZNF574 Promotes Ovarian Cancer Cell Proliferation and Migration through Regulating AKT and AMPK Signaling Pathways

Ovarian cancer is the most common malignancy in females. Despite improvements in therapeutic technologies, patients with ovarian cancer face poor prognoses. Studies have reported that ZNF574 is an oncogene in colorectal cancers. However, the role of ZNF574 in ovarian cancer has not been evaluated. We investigated the role of ZNF574 in ovarian cancer.The expression of ZNF574 was silenced using siRNA. The expression of ZNF574 was detected using qRT-PCR and western blot. Cell viability was evaluated using the CCK8 and colony formation assays. The cell cycle and apoptosis were evaluated using flow cytometry. Transwell assay was used to evaluate cell migration.We showed that ZNF574 was upregulated in ovarian cancer, and patients with high ZNF574 expression had shorter overall survival. We found that ZNF574 knockdown inhibited cell proliferation and migration, whereas ZNF574 overexpression promoted cell proliferation and migration. In addition, ZNF574 knockdown promoted apoptosis of ovarian cells and arrested the cell cycle. Knockdown of ZNF574 enhanced cisplatin toxicity, which indicated that knockdown of ZNF574 could allow for treatment with reduced doses of cisplatin, resulting in fewer adverse reactions. Protein levels of phosphorylated AKT were decreased and levels of phosphorylated AMPKα were increased in ZNF574-knockdown ovarian cancer cells.These results indicated that ZNF574 may function as an oncogene in ovarian cancer through regulation of the AKT and AMPK signaling pathways. Furthermore, ZNF574 may be a prognostic indicator and therapeutic target for ovarian cancer.