PTEN/AKT and Wnt/β-catenin signaling pathways regulate the proliferation of Lgr5+cells in liver cancer

被引:15
|
作者
Han, Jia [1 ,2 ]
Han, Jimin [3 ]
Lin, Kaijun [3 ]
Wang, Jingru [3 ]
Li, Guiqiang [3 ]
Li, Xiaohong [1 ]
Gao, Ying [1 ,2 ]
机构
[1] Bengbu Med Coll, Affiliated Hosp 1, Dept Anesthesiol, Bengbu, Anhui, Peoples R China
[2] First Peoples Hosp Foshan, Dept Anesthesiol, Foshan, Peoples R China
[3] Sun Yat Sen Univ, Sch Pharmaceut Sci Shenzhen, Shenzhen, Guangdong, Peoples R China
关键词
Cancer stem cells; Lgr5; PTEN; beta-catenin; Liver cancer; ANTIBODY-DRUG CONJUGATE; HEPATOCELLULAR-CARCINOMA; STEM-CELLS; RISK; LGR5; EPIDEMIOLOGY; MAINTENANCE; EXPANSION; TUMORS; SHP2;
D O I
10.1016/j.bbrc.2023.10.049
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The progression and spread of tumors are believed to be primarily caused by cancer stem cells (CSCs). Nevertheless, the task of focusing on CSCs for cancer treatment continues to be difficult. Lgr5, a G-protein-coupled receptor containing leucine-rich repeats, is highly expressed in different types of cancer and serves as a distinctive marker for cancer stem cells (CSCs). In this study, we employed the Cre-loxP system and Lgr5 tracking mice of male to selectively remove PTEN and beta-catenin in Lgr5+ cells of DEN-induced liver cancer and monitor the behavior of Lgr5+ cells. The tracking data revealed that the activation of PTEN-mediated AKT signaling in Lgr5 led to a significant rise in the quantity of Lgr5+ cells, whereas the inhibition of Wnt/beta-catenin signaling decreased the number of cells in DEN-induced liver cancer. Therefore, we have shown that the growth of Lgr5+ cells can be controlled by the PTEN/AKT and Wnt/beta-catenin pathways, offering a potential treatment option for fighting against liver cancer.
引用
收藏
页数:6
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