Abstract

Ovarian cancer is one of the most common malignancies of the female reproductive system, with the second-highest incidence and the most lethality of female malignancies. Due to the lack of reliable biomarkers, 70% of ovarian cancer patients are already in advanced stages when diagnosed, while the 5-year survival rate is less than 50%. Therefore, it is a hot spot in ovarian cancer research to explore new diagnostic indicators and therapeutic targets assisted by early pathological molecular biology and to develop targeted drugs. LncRNA MAFG-AS1 promotes tumor growth in multiple cancers. However, the function of MAFG-AS1 in ovarian cancer has not been declared. Here, we explore the function and mechanism of MAFG-AS1 in ovarian cancer. MAFG-AS1 levels were upregulated in tumor tissues than adjacent normal tissues isolated from ovarian cancer patients. Silencing of MAFG-AS1 prevented cell proliferation, migration and invasion in ovarian cancer cells. Furthermore, we declared that MAFG-AS1 knockdown reduced autophagy, inhibited epithelial-mesenchymal transition in SKOV3 cells. MiR-24-3p, B4GAT1, the downstream target of MAFG-AS1 was verified by luciferase. Taken together, our research demonstrated the mechanism of MAFG-AS1 in ovarian cancer. MAFG-AS1 knockdown could prevent tumor development by inhibiting autophagy and the epithelial-mesenchymal transition pathway.