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Article type: Research Article
Authors: Jin, Hua | Kim, Hyun-Woo | Xu, Cheng-Xiong | Kwon, Jung-Taek | Hwang, Soon-Kyung | Lee, Eun-Sun | Chang, Seung-Hee | Park, Sung-Jin | Noh, Mi-Suk | Woo, Min-Ah | Yu, Kyeong-Nam | Lee, Hu-Jang | Choi, Joon-Weon | Choi, Don-Ha | Cho, Myung-Haing
Affiliations: Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea | Institute of Animal Medicine, College of Veterinary Medicine, Kyeongsang National University, Chinju 600-701, Korea | Division of Wood Chemistry & Microbiology, Korea Forest Research Institute, Seoul 130-712, Korea
Note: [] Corresponding authors: Don-Ha Choi, Ph.D., Division of Wood Chemistry and Microbiology, Korea Forest Research Institute, 207 Cheongnyangni-Dong, Dongdaemun-Gu, Seoul 130-712, Korea. E-mail: cdonha@foa.go.kr. Or Myung-Haing Cho, Ph.D., Laboratory of Toxicology, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea. E-mail: mchotox@snu.ac.kr
Abstract: Previously we reported that cadalene extracted from Zelkova serrata inhibited lung tumorigenesis in mice. However, the precise mechanism has not yet investigated. Here, we examined the effects of cadalene on signal pathways important for apoptosis, cell cycle, and protein translation in lung cancer cells. Our results showed that cadalene suppressed the expression of Akt and its phosphor-forms through controlling PI3K and PTEN. Cadalene also induced apoptosis through facilitating pro-apoptotic protein expression. In addition, cadalene caused cell cycle arrest and decreased mTOR-mediated protein translation. Taken together, cadalene may be developed as a lung cancer therapeutic agent in the future.
Keywords: Cadalene, lung cancer, apoptosis, cell cycle, protein translation
Journal: BioFactors, vol. 29, no. 2-3, pp. 67-75, 2007
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