Actin Gamma Smooth Muscle 2 Promotes Epithelial Ovarian Cancer Cell Proliferation via the AKT1/NF-κB Signaling Pathway

Abstract

Epithelial ovarian cancer (EOC) is associated with high mortality rates worldwide and is characterized as the most lethal gynecological cancer. The study aimed to investigate the functional role and underlying molecular mechanism of actin gamma smooth muscle 2 (ACTG2) in the progression of EOC. Data mining from The Cancer Genome Atlas (TCGA) databases showed the expression of ACTG2 was significantly upregulated in EOC and negatively associated with longer overall survival and better prognosis of patients. By using of gain-of-function and loss-of-function experiments in vitro and in vivo, we found that ACTG2 promoted EOC cell proliferation and suppressed cell apoptosis. Mechanistic study revealed that ACTG2 regulates EOC cell proliferation by activating the AKT serine/threonine kinase 1 (AKT1)/nuclear factor-κB (NF-κB) signaling pathway. Importantly, p65 plays a crucial role in this newly identified regulatory mechanism. Our findings demonstrate that ACTG2 may play an oncogenic role in EOC, suggesting its potential as a therapeutic target.