Baicalein enhanced cisplatin sensitivity of gastric cancer cells by inducing cell apoptosis and autophagy via Akt/mTOR and Nrf2/Keap 1 pathway
Baicalein enhanced cisplatin sensitivity of gastric cancer cells by inducing cell apoptosis and autophagy via Akt/mTOR and Nrf2/Keap 1 pathway
复制标题
黄芩素通过 Akt/mTOR 和 Nrf2/Keap 1 通路诱导细胞凋亡和自噬增强胃癌细胞顺铂敏感性
DOI：
10.1016/j.bbrc.2020.07.045
复制
发表时间：
2020-10-20
影响因子：
3.1
通讯作者：
Tie, Jun
中科院分区：
文献类型：
--
作者：
Li, Ping;Hu, Jianran;Tie, Jun
Baicalein is a natural flavonoid with various pharmacological activities including antitumor. The synergistic anti-cancer effect of the combination of baicalein and Cisplatin (DDP) on gastric cancer (GC) has not been reported. MTT assay and colony formation assay were used to determine the inhibitory effect of the combination of baicalein and DDP on cell survival. Invasive assay was performed to test the effects of baicalein and DDP on cell invasive capability. A flow cytometric analysis was conducted to determine the apoptosis-induced effects of baicalein on GC cells, especially SGC-7901/DDP (resistant to DDP). Confocal laser microscope and real-time PCR were used to test autophagy-induced effects of baicalein on SGC7901 and SGC-7901/DDP cells. Western blotting was performed to investigate the molecular mechanisms of baicalein inducing apoptosis and autophagy. Our study showed that baicalein could inhibit cell proliferation of MGC-803, HGC-27, SGC-7901 and SGC-7901/DDP, and the inhibitory effect was extremely enhanced when combining with DDP. Additionally, combination of baicalein and DDP suppressed the invasive capability and induced apoptosis and autophagy in both SGC-7901 and SGC-7901/DDP, and the effect was stronger than that of DDP or baicalein alone. The further molecular mechanism analysis indicated that baicalein modulated the activities of Akt/mTOR and Nrf2/Keap 1 signaling. Our study demonstrated that baicalein enhanced DDP sensitivity of SGC-7901/DDP gastric cancer cells by inducing apoptosis and autophagy via Akt/mTOR and Nrf2/Keap 1 pathway. (C) 2020 Elsevier Inc. All rights reserved.
