蛋白激酶B
PI3K/AKT/mTOR通路
CTD公司
斑蝥素
信号转导
细胞迁移
癌症研究
化学
细胞凋亡
细胞生物学
生物
细胞
生物化学
海洋学
地质学
有机化学
作者
Mengyun Song,Xianfei Wang,Yajun Luo,Haohuan Li,Tan Wang,Pengcheng Ye,Zhiming Fu,Fei Lu,Wanping Xiang,Linghan Tang,Yao Lin,Yuqiang Nie,Jiangwei Xiao
标识
DOI:10.1016/j.cbi.2020.108939
摘要
Cantharidin (CTD) is a traditional Chinese medicine that shows an anticancer effects in multiple types of cancer cells. However, the mechanism of CTD anti-cancer function in gastric cancer (GC) is still unclear. The aim of the present study was to investigate the underlying mechanism that CTD inhibits proliferation and migration through suppression of the PI3K/Akt signaling. CTD induced GC cell apoptosis and inhibited metastasis measured by CCK8 assays as well as wound healing assays and transwell assays. Mechanistic investigations suggested that CTD modulated the PI3K/Akt signaling via western-blot and quantitative q-PCR. In addition, we identified and confirmed CCAT1 as a novel direct target of CTD inhibited PI3K/AKt signaling expression. In conclusion, our results provide new point into the critical role of CTD in suppressing PI3K/Akt signaling via down-regulation of CCAT1, resulting in suppression GC cell growth and migration/invasion.
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