Cytisine exerts anti-tumour effects on lung cancer cells by modulating reactive oxygen species-mediated signalling pathways

Cytisine is a natural product isolated from plants and is a member of the quinolizidine alkaloid family. This study aims to investigate the effect of cytisine in human lung cancer. Cell viability was determined using the CCK-8 assay, and the results showed that cytisine inhibited the growth of lung...

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Published in:Artificial cells, nanomedicine, and biotechnology nanomedicine, and biotechnology, 2020-01, Vol.48 (1), p.84-95
Main Authors: Xu, Wan-Ting, Li, Tian-Zhu, Li, Shu-Mei, Wang, Cheng, Wang, Hao, Luo, Ying-Hua, Piao, Xian-Ji, Wang, Jia-Ru, Zhang, Yu, Zhang, Tong, Xue, Hui, Cao, Long-Kui, Jin, Cheng-Hao
Format: Article
Language:English
Subjects:
AKT protein
Anticancer properties
Apoptosis
Bcl-2 protein
Carcinogenesis
Carcinogens
Caspase-3
Cell cycle
cell cycle arrest
Cell viability
Cholecystokinin
Cytisine
Flow cytometry
human lung cancer cell
Lung cancer
Membrane potential
Mitochondria
Natural products
NF-κB protein
Phosphorylation
Poly(ADP-ribose) polymerase
Reactive oxygen species
Signal transduction
Signaling
Stat3 protein
Tumor cell lines
Tumorigenesis
Tumors
Xenografts
Xenotransplantation
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Summary:Cytisine is a natural product isolated from plants and is a member of the quinolizidine alkaloid family. This study aims to investigate the effect of cytisine in human lung cancer. Cell viability was determined using the CCK-8 assay, and the results showed that cytisine inhibited the growth of lung cancer cell lines. The apoptotic effects were evaluated using flow cytometry, and the results showed that cytisine induced mitochondrial-dependent apoptosis through loss of the mitochondrial membrane potential; increased expression of BAD, cleaved caspase-3, and cleaved-PARP; and decreased expression levels of Bcl-2, pro-caspase-3, and pro-PARP. In addition, cytisine caused G2/M phase cell cycle arrest that was associated with inhibiting the AKT signalling pathway. During apoptosis, cytisine increased the phosphorylation levels of JNK, p38, and I-κB, and decreased the phosphorylation levels of ERK, STAT3, and NF-κB. Furthermore, cytisine treatment led to the generation of ROS, and the NAC attenuated cytisine-induced apoptosis. In vivo, cytisine administration significantly inhibited the lung cancer cell xenograft tumorigenesis. In conclusion, cytisine plays a critical role in suppressing the carcinogenesis of lung cancer cells through cell cycle arrest and induction of mitochondria-mediated apoptosis, suggesting that it may be a promising candidate for the treatment of human lung cancer.
ISSN:2169-1401
2169-141X
DOI:10.1080/21691401.2019.1699813