表皮生长因子受体
细胞凋亡
下调和上调
癌症研究
蛋白激酶B
肺癌
药理学
程序性细胞死亡
PI3K/AKT/mTOR通路
受体
化学
医学
内科学
生物化学
基因
作者
Zheng-Hong Zhong,Zelin Yi,Yidan Zhao,Jue Wang,Ze‐Bo Jiang,Cong Xu,Ya-Jia Xie,Qi-da He,Zi-yan Tong,Xiaojun Yao,Elaine Lai‐Han Leung,Paolo Coghi,Xing‐Xing Fan,Min Chen
摘要
Lung cancer is the leading cause of cancer death. Pyronaridine, a synthetic drug of artemisinin, has been used in China for over 30 years for the treatment of malaria, but its effect on non-small cell lung cancer (NSCLC) cells is rarely reported. In this study, we determined the efficacy of pyronaridine in four different NSCLC cell lines and explored its mechanism in H1975. The data showed that pyronaridine could upregulate the expression of TNF-related apoptosis-inducing ligand (TRAIL)-mediated death receptor 5 to promote cellular apoptosis. Meanwhile, the JNK (c-Jun N-terminal kinase) level was detected to be significantly increased after treating with pyronaridine. We used JNK inhibitor and found that it could partially inhibit cell apoptosis. The results showed that epidermal growth factor receptor (EGFR), PI3K, and AKT were downregulated after the treatment of pyronaridine. In summary, pyronaridine can selectively kill NSCLC by regulating TRAIL-mediated apoptosis and downregulating the protein level of EGFR. It is a promising anticancer drug for NSCLC.
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