Xanthones from the Leaves of Garcinia cowa Induce Cell Cycle Arrest, Apoptosis, and Autophagy in Cancer Cells
Zhengxiang Xia,
Hong Zhang,
Danqing Xu,
Yuanzhi Lao,
Wenwei Fu,
Hongsheng Tan,
Peng Cao,
Ling Yang,
Hongxi Xu
Affiliations
Zhengxiang Xia
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Hong Zhang
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Danqing Xu
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Yuanzhi Lao
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Wenwei Fu
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Hongsheng Tan
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Peng Cao
Jiangsu Province Academy of Traditional Chinese Medicine, No. 100 Shizi Street, Hongshan Road, Nanjing 210028, China
Ling Yang
Laboratory of Pharmaceutical Resource Discovery, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, 457 Zhong-shan Road, Dalian 116023, China
Hongxi Xu
School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
Two new xanthones, cowaxanthones G (1) and H (2), and 23 known analogues were isolated from an acetone extract of the leaves of Garcinia cowa. The isolated compounds were evaluated for cytotoxicity against three cancer cell lines and immortalized HL7702 normal liver cells, whereby compounds 1, 5, 8, and 15–17 exhibited significant cytotoxicity. Cell cycle analysis using flow cytometry showed that 5 induced cell cycle arrest at the S phase in a dose-dependent manner, 1 and 16 at the G2/M phase, and 17 at the G1 phase, while 16 and 17 induced apoptosis. Moreover, autophagy analysis by GFP-LC3 puncta formation and western blotting suggested that 17 induced autophagy. Taken together, our results suggest that these xanthones possess anticancer activities targeting cell cycle, apoptosis, and autophagy signaling pathways.
