细胞周期
A549电池
MAPK/ERK通路
自噬
下调和上调
细胞周期检查点
细胞凋亡
细胞生长
细胞生物学
流式细胞术
化学
免疫印迹
癌症研究
MTT法
生物
分子生物学
信号转导
生物化学
基因
作者
Jinhua Chen,Qingfeng Guo,Jinxiang Zhang,Zhanhua Yin,Wenping Song,Baoxia He,Yongna Zhang,Wenzhou Zhang,Lin Chen
摘要
Chaetoglobosin G (CG) is a fungal secondary metabolite and shows anti-tumor effects. However, the mechanisms behind the anti-tumor effect is still unclear. In this study, we evaluated the anti-proliferation effect of CG on human NSCLC A549 cells and explored the underlying mechanisms. The anti-proliferation effect of CG on A549 cells was evaluated by MTT. The targets of CG were screened through transcriptome sequencing. A flow cytometer was used to detect cell cycle and apoptosis. Western blotting was used to analyze apoptosis, cell cycle and autophagy related protein expression. Our results showed that CG had a dose-dependent inhibitory effect on proliferation of A549 cells. Transcriptome sequencing analysis found that CG obviously induced cell cycle arrest. Flow cytometry analysis and western blot showed that CG induced G2/M arrest with p21 protein upregulation and cyclinB1 protein downregulation. Western blot analysis also indicated that p-EGFR, EGFR, p-MEk and p-ERK protein expressions decreased and autophagy protein LC3II expression increased, indicating that CG can promote autophagy through EGFR/MEK/ERK/LC3 pathway. Moreover, CG can induce apoptosis with bcl-2 protein decrease. In conclusion, this study indicated that CG obviously inhibited A549 cell proliferation, and its mechanism may induce autophagy of A549 cells through EGFR/MEK/ERK/LC3 pathway to upregulate the expression of P21, thus lead to G2/M phase arrest to exert an anti-tumor role.
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