PI3K/AKT/mTOR通路
细胞凋亡
蛋白激酶B
细胞周期蛋白依赖激酶1
细胞周期
癌症研究
细胞生长
细胞
免疫印迹
化学
分子生物学
生物
医学
内科学
生物化学
基因
作者
Shuhan Wang,Qixiao Cui,Xiaoyu Chen,Xuejie Zhu,Kehao Lin,Qiusheng Zheng,Yuliang Wang,Defang Li
摘要
. Here, we showed that AIL inhibited the proliferation of human TSCC, the cell viability of Cal-27 and Tca8113 was significantly decreased after AIL treatment for 24 h. Hoechst 33258 staining demonstrated apoptotic characteristics (such as chromatin aggregation) after AIL treatment. The ratio of early- and late-apoptotic cells in AIL-treated Cal-27 and TCA8113 cells increased remarkably when compared with the control group. Bcl-2/Bax ratio and the levels of PARP1, caspase-9, and caspase-3 decreased after AIL treatment, accompanied by significant increase of cleaved PARP1, cleaved caspase-9, and caspase-3 in Cal-27 and TCA8113 cells. Meanwhile, AIL led to Cal-27 cell cycle arrest at G2/M phase. Western blot implied decreased levels of CDK1 and cyclin B1 after AIL treatment. The level of phospho-PI3K p55 subunit and p-Akt were significantly downregulated by AIL in both Cal-27 and TCA8113 cells. These findings implied the potential applications of AIL in the treatment of human TSCC.
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