PI3K/AKT/mTOR通路
蛋白激酶B
细胞周期
细胞生长
癌症研究
肝癌
癌症
生物
肝细胞癌
信号转导
细胞生物学
生物化学
遗传学
作者
Ang Li,Chenglin Qin,H Chen,Yong Zhou,Yuping Xu,Min Xu,Wenzhang Zha
标识
DOI:10.1166/jbn.2024.3815
摘要
Hepatocellular carcinoma (HCC) is a major contributor to global cancer-related deaths. The chromatin binding protein MCM5, part of the MCM family, plays a crucial role in regulating DNA replication, a key driver of cancer. Database analysis revealed elevated MCM5 levels in HCC, associated with shorter patient survival. Silencing MCM5 impedes liver cancer cell proliferation by halting the cell cycle at G1 phase. In vivo experiments confirm this effect, demonstrating that MCM5 knockdown suppresses HCC growth. Mechanistic studies unveil MCM5′s impact on HCC development via the PI3K/AKT/mTOR signaling pathway. Reversing liver cancer growth is possible by adding AKT agonist SC79. Additionally, inhibiting mettl3 with stm2457 downregulates MCM5, further suppressing liver cancer growth. In summary, high MCM5 expression in liver cancer correlates with poor prognosis and drives disease progression. Targeting MCM5 with mettl3 inhibitors presents a promising therapeutic strategy for HCC.
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