Cytisine exerts anti-tumour effects on lung cancer cells by modulating reactive oxygen species-mediated signalling pathways. Issue 1 (1st January 2020)

• Record Type: Journal Article
• 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
• Is Part Of: Artificial cells, nanomedicine, and biotechnology. Volume 48:Issue 1(2020)
• Page Start: 84
• Page End: 95
• Publication Date: 2020-01-01
• Subjects: Cytisine -- human lung cancer cell -- apoptosis -- cell cycle arrest -- reactive oxygen species; Artificial cells -- Periodicals; Nanotechnology -- Periodicals; Blood substitutes -- Periodicals; Tissue engineering -- Periodicals; Molecules -- Periodicals; Biotechnology -- Periodicals; 615.39
• DOI: 10.1080/21691401.2019.1699813
• Languages: English
• ISSNs: 2169-1401

Abstract

Abstract: 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.