黄芩素
顺铂
PI3K/AKT/mTOR通路
A549电池
上皮-间质转换
蛋白激酶B
化学
细胞凋亡
癌症研究
NF-κB
药理学
医学
下调和上调
生物化学
内科学
化疗
基因
作者
Man Yu,Ben-Quan Qi,Xiao-xiang Wu,Jian Xu,Xiaolin Liu
标识
DOI:10.1016/j.biopha.2017.04.001
摘要
Baicalein, a bioactive flavonoid, exhibits anti-inflammatory and anti-cancer activities. However, few studies reported the interaction of baicalein with chemotherapeutic agents. Our study showed that baicalein significantly enhanced the chemosensitivity of cisplatin (CDDP) in vivo and in vitro. We found that A549/CDDP (resistant to CDDP) cells not only acquired epithelial-mesenchymal transition (EMT) phenotype, but also showed increased NF-κB activity compared with A549 cells (sensitive to CDDP). Our study further demonstrated that PI3K/Akt/NF-κB pathway controlled CDDP resistance via EMT and NF-κB–mediated apoptosis. Baicalein significantly suppressed the PI3K/Akt/NF-κB pathway, leading to conversion of EMT to mesenchymal-epithelial transition (MET, the reciprocal mesenchymal to epithelial transition), and inhibition of NF-κB-mediated antiapoptotic proteins in A549/CDDP cells. In conclusion, our study demonstrated that baicalein reversed the resistance of human A549 lung adenocarcinoma cells to cisplatin by inhibiting EMT and attenuating apoptosis via PI3K/Akt/NF-κB pathway.
科研通智能强力驱动
Strongly Powered by AbleSci AI