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Ling-Qi Meng, Yue Wang, Ying-Hua Luo, Xian-Ji Piao, Chang Liu, Yue Wang, Yi Zhang, Jia-Ru Wang, Hao Wang, Wan-Ting Xu, Yang Liu, Yi-Qin Wu, Hu-Nan Sun, Ying-Hao Han, Mei-Hua Jin, Gui-Nan Shen, Nan-Zhu Fang, Cheng-Hao Jin
(Department of Biochemistry and Molecular Biology, College of Life Science and Technology, Heilongjiang Bayi Agricultural University, Daqing, Heilongjiang, China (mainland))
Med Sci Monit 2018; 24: LBR3710-3719
Quinalizarin (1,2,5,8-tetrahydroxyanthraquinone) exhibits potentially useful anticancer effects by inducing apoptosis in several types of cancer, but its underlying mechanism of action remains unknown. The present study examined the effects of quinalizarin on the induction of cell cycle arrest, apoptosis, the generation of reactive oxygen species (ROS), other underlying mechanisms, and its role in modifying colorectal cancer cell lines.
MATERIAL AND METHODS: The MTT assay was used to evaluate the viability of SW480 and HCT-116 cells that had been treated with quinalizarin and 5-fluorouracil (5-FU). Cell cycle arrest and apoptosis were analyzed by flow cytometry. Western blotting was used to investigate the mitochondrial pathway; Akt, MAPK, and STAT3 signaling pathways were also investigated. The relationship between ROS generation and apoptosis was analyzed by flow cytometry and western blotting.
RESULTS: The results indicated that quinalizarin significantly inhibits the viability of SW480 and HCT-116 cells in a dose-dependent manner. Quinalizarin induced SW480 cell cycle arrest at G2/M by regulating cyclin B1 and CDK1/2. The apoptosis-related protein expression levels of p-p53, Bad, cleaved caspase-3, cleaved PARP and p-JNK were increased in quinalizarin-treated cells, while protein expression levels Bcl-2, p-Akt, p-ERK, and p-STAT3 were decreased. Quinalizarin induced apoptosis in colorectal cancer cells by regulating MAPK and STAT3 signaling pathways via ROS generation.
CONCLUSIONS: Quinalizarin induces apoptosis via ROS-mediated MAPK/STAT3 signaling pathways.