In vitro antitumor effect of cucurbitacin E on human lung cancer cell line and its molecular mechanism.
10.1016/S1875-5364(20)30058-3
- Author:
Si-Yuan JING
1
;
Zi-Dan WU
1
;
Tie-Hua ZHANG
1
;
Jie ZHANG
2
,
3
;
Zheng-Yi WEI
3
,
4
Author Information
1. College of Food Science and Engineering, Jilin University, Changchun 130062, China.
2. College of Food Science and Engineering, Jilin University, Changchun 130062, China. Electronic address: zhangjjlu@
3. com.
4. Institute of Agricultural Biotechnology, Jilin Academy of Agricultural Sciences, Changchun 130033, China. Electronic address: weizy80@
- Publication Type:Journal Article
- Keywords:
Antitumor effect;
Apoptosis;
Cell cycle arrest;
Cucurbitacin E;
Lung cancer cell
- From:
Chinese Journal of Natural Medicines (English Ed.)
2020;18(7):483-490
- CountryChina
- Language:English
-
Abstract:
Cucurbitacin E (CuE) is previously reported to exhibit antitumor effect by several means. In this study, CuE acted as a tyrosine kinase inhibitor interfering with the epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) signaling pathway and subsequently induced apoptosis and cell cycle arrest in non-small-cell lung cancer (NSCLC) cell line A549. The apoptosis regulators, cleaved Caspases-3 and Caspases-9, were observed to be increased with the treatment of CuE. The activated transcription factor STAT3 and the apoptosis inhibitor protein survivin were also observed to be reduced. The cell cycle regulators, CyclinA2, cylinB1, CyclinD1 and CyclinE, were also investigated and the results suggested that the cell cycle was arrested at G1/G0 phase. Treatment of CuE also altered the existence status of most of the participants in the EGFR/MAPK signaling. Phosphorylation of EGFR enhanced significantly, leading to the alteration of members downstream, either total amount or phosphorylation level, notably, MEK1/2 and ERK1/2. Moreover, the results of molecular simulation brought an insight on the interaction mechanism between CuE and EGFR. In summary, CuE exhibited anti-proliferative effect against A549 cells by targeting the EGFR/MAPK signaling pathway.
