Anticancer Activity and Mode of Action of Cu(II), Zn(II), and Mn(II) Complexes with 5-Chloro-2-<i>N</i>-(2-quinolylmethylene)aminophenol
Shuangshuang Gai,
Liqin He,
Mingxian He,
Xuwei Zhong,
Caiyun Jiang,
Yiming Qin,
Ming Jiang
Affiliations
Shuangshuang Gai
Key Laboratory for Zhuang and Yao Pharmaceutical Quality Biology, School of Food and Biochemical Engineering, Guangxi Science & Technology Normal University, Laibin 546199, China
Liqin He
Key Laboratory for Zhuang and Yao Pharmaceutical Quality Biology, School of Food and Biochemical Engineering, Guangxi Science & Technology Normal University, Laibin 546199, China
Mingxian He
Key Laboratory for Zhuang and Yao Pharmaceutical Quality Biology, School of Food and Biochemical Engineering, Guangxi Science & Technology Normal University, Laibin 546199, China
Xuwei Zhong
Key Laboratory for Zhuang and Yao Pharmaceutical Quality Biology, School of Food and Biochemical Engineering, Guangxi Science & Technology Normal University, Laibin 546199, China
Caiyun Jiang
Key Laboratory for Zhuang and Yao Pharmaceutical Quality Biology, School of Food and Biochemical Engineering, Guangxi Science & Technology Normal University, Laibin 546199, China
Yiming Qin
Key Laboratory for Zhuang and Yao Pharmaceutical Quality Biology, School of Food and Biochemical Engineering, Guangxi Science & Technology Normal University, Laibin 546199, China
Ming Jiang
Key Laboratory for Zhuang and Yao Pharmaceutical Quality Biology, School of Food and Biochemical Engineering, Guangxi Science & Technology Normal University, Laibin 546199, China
Developing a new generation of anticancer metal-based drugs that can both kill tumor cells and inhibit cell migration is a promising strategy. Herein, we synthesized three Cu(II), Zn(II), and Mn(II) complexes derived from 5-chloro-2-N-(2-quinolylmethylene)aminophenol (C1–C3). Among these complexes, the Cu(II) complex (C1) showed significantly greater cytotoxicity toward lung cancer cell lines than cisplatin. C1 inhibited A549 cell metastasis and suppressed the growth of the A549 tumor in vivo. In addition, we confirmed the anticancer mechanism of C1 by triggering multiple mechanisms, including inducing mitochondrial apoptosis, acting on DNA, blocking cell cycle arrest, inducing cell senescence, and inducing DNA damage.
