生存素
细胞凋亡
癌症研究
细胞周期蛋白D1
细胞周期
A549电池
细胞周期蛋白B1
腺癌
克隆形成试验
程序性细胞死亡
化学
细胞生长
细胞周期检查点
下调和上调
生物
癌症
细胞周期蛋白依赖激酶1
基因
生物化学
遗传学
作者
Bilal Rah,Jasmin Shafarin,Mawieh Hamad,Jibran Sualeh Muhammad
摘要
Sclareol (SC) has shown significant anticancer activity against breast and colon cancers among others. However, its ability to precipitate similar anticancer effects in lung cancer has yet to be investigated. To address this issue, SC-treated lung adenocarcinoma cells (A549) were assessed for viability and functional competence as well as the expression of genes related to apoptosis and cell cycling. Our results demonstrated that SC treatment inhibited A549 cell clonogenic features and reduced their migration and invasion potential in a dose-dependent manner. Mechanistically, SC treatment downregulated the expression of cyclin D1 and survivin and upregulated that of p21 and p16, which was associated with a significant increase in the percentage of SubG0 cells. SC treatment is also associated with the induction of both the extrinsic and intrinsic apoptotic pathways, as evidenced by the increased expression and splitting of PARP1 and procaspases 3 and 9 and the reduced expression of antiapoptotic proteins Bcl-2 and Bcl-xL. Increased cell death in SC-treated cells is likely to have resulted from the induction of ferroptosis as suggested by the reduced expression of FPN and the inhibition of the anti-ferroptosis regulator GPX4. In conclusion, the data presented here suggest that SC can reduce lung carcinoma cell growth and metastasis and promote cell death.
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