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Research articles

ScienceAsia 47 (2021): 11-18 |doi: 10.2306/scienceasia1513-1874.2021.001


Ginkgolic acid inhibits proliferation and migration of human hepatocellular carcinoma cells by inducing G0/G1 cell cycle arrest


Jiayu Chena,b, Rui Wanga, Ying Lia,c, Chunhe Lid, Tao Liud, Yi Xine, Yiling Lib,*, Dianbao Zhanga,*

 
ABSTRACT:     Hepatocellular carcinoma (HCC) is a common cancer worldwide with high morbidity and mortality. Ginkgolic acid (GA) is a natural compound obtained from leaves and seed coats of Ginkgo biloba L., and it has been reported to have various bioactivities. However, the effects of GA on HCC cell cycle distribution and the mechanisms involved are still unknown. By CCK-8 assay and Transwell assay, the cell viability and migration of HCC cells were shown to be inhibited significantly by GA in a concentration-dependent manner. By cell cycle analysis and western blot, the cell cycle arrest at G0/G1 phase was shown to contribute to the inhibitory effects of GA. Furthermore, the phosphorylation of p38 MAPK was found to be elevated upon GA treatment as analyzed by western blot. Thus, GA inhibited cell proliferation and migration of HCC cells by inducing G0/G1 cell cycle arrest via p38 MAPK activation, indicating GA as an agent candidate for HCC treatment.

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a Department of Stem Cells and Regenerative Medicine, Key Laboratory of Cell Biology, National Health Commission of China and Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang 110122 China
b Department of Medicine, Division of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110015 China
c Department of Pathology, Affiliated Hospital of Jining Medical University, Jining 272029 China
d Department of Natural Products Chemistry, School of Pharmacy, China Medical University, Shenyang 110122 China
e School of Management, Tianjin University of Traditional Chinese Medicine, Tianjin 301617 China

* Corresponding author, E-mail: zhangdianbao@gmail.com, lyl-72@163.com

Received 20 Jul 2020, Accepted 26 Oct 2020