AKT1型
AKT2型
蛋白激酶B
癌症研究
细胞生长
卵巢癌
下调和上调
细胞凋亡
信号转导
生物
细胞生物学
癌症
基因
遗传学
作者
Yinjue Yu,Jiangxia Li,Xiaohang Wang,Xiaoxiao Li,Cuiting Lyu,Lina Yang,Yongrui Bai
摘要
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.
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