| Literature DB >> 31945315 |
Mengyun Song1, Xianfei Wang2, Yajun Luo2, Zilin Liu2, Wang Tan2, Pengcheng Ye2, Zhiming Fu3, Fei Lu2, Wanping Xiang2, Linghan Tang2, Lin Yao2, Yuqiang Nie4, Jiangwei Xiao5.
Abstract
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.Entities:
Keywords: CCAT1; Cantharidin; Gastric cancer; Long non-coding RNA; PI3K/AKt
Mesh:
Substances:
Year: 2020 PMID: 31945315 DOI: 10.1016/j.cbi.2020.108939
Source DB: PubMed Journal: Chem Biol Interact ISSN: 0009-2797 Impact factor: 5.192