青蒿琥酯
PI3K/AKT/mTOR通路
蛋白激酶B
癌症研究
癌变
癌症
脉络膜黑色素瘤
信号转导
黑色素瘤
医学
化学
内科学
免疫学
生物化学
恶性疟原虫
疟疾
作者
Ningning Yao,Qingyue Ma,Wendan Yi,Yichong Liu,Qian Zhang,Xiaodi Gao,Xintong Zhao,Haowen Wang,Ke Lei,Aihua Sui,Wenjuan Luo
出处
期刊:Cytokine
[Elsevier BV]
日期:2024-09-27
卷期号:184: 156771-156771
被引量:1
标识
DOI:10.1016/j.cyto.2024.156771
摘要
The impact of Ang-1 on tumors remains a subject of contention, with its mechanism of action exhibiting complexity in the progression of diverse tumor types. Ang-1 has been shown to promote the progression of glioma, glioma, esophageal and human cervical cancer, whereas it exerts inhibitory effects on the growth of breast and colon cancer. However, the specific function of Ang-1 in CM has not been clarified. This research aims to explore the function of Ang-1 on CM and the underlying mechanism. WB and qPCR were utilized to measure the expression levels of different factors in CM cells. Clonogenic, CCK-8 and Transwell migration assay were used to probe CM cells' proliferation and migration ability. Xenograft tumor model was used to testify the effect of Ang-1 and Artesunate (ART) on the growth of CM in vivo. We found Ang-1 promoted CM proliferation and migration, while it was inhibited by ART in vitro. Moreover, both ART treatment and Ang-1 knockdown had the effect of suppressing tumor growth in CM xenograft model. Mechanically, Ang-1 activated Akt/mTOR pathway and induced epithelial-mesenchymal transition (EMT) in CM cells. Furthermore, ART regulated Akt/mTOR pathway by decreasing the expression of Ang-1 in CM cells. Ang-1 promotes tumorigenesis of CM by regulating Akt/mTOR pathway, which can be inhibited by ART.
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