Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis
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Jiguang Ma1,*, Wanxing Duan1,*, Suxia Han1, Jianjun Lei2, Qinhong Xu2, Xin Chen2, Zhengdong Jiang2, Ligang Nan2, Jiahui Li2, Ke Chen2, Liang Han2 Zheng Wang2, Xuqi Li3, Erxi Wu4, Xiongwei Huo3
1 Department of Oncology, First Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China
2 Department of Hepatobiliary Surgery, First Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China
3 Department of General Surgery, First Affiliated Hospital, Xi’an Jiaotong University, Xi’an, China
4 Department of Pharmaceutical Sciences, North Dakota State University, Fargo, ND, USA
* These authors have contributed equally to this work
Suxia Han, email:
Xiongwei Huo, email:
Keywords: lipogenesis, cancer metabolism, ginkgolic acid (GA), AMP-activated protein kinase (AMPK), pancreatic cancer
Received: January 26, 2015 Accepted: February 28, 2015 Published: March 26, 2015
Ginkgolic acid (GA) is a botanical drug extracted from the seed coat of Ginkgo biloba L. with a wide range of bioactive properties, including anti-tumor effect. However, whether GA has antitumor effect on pancreatic cancer cells and the underlying mechanisms have yet to be investigated. In this study, we show that GA suppressed the viability of cancer cells but has little toxicity on normal cells, e.g, HUVEC cells. Furthermore, treatment of GA resulted in impaired colony formation, migration, and invasion ability and increased apoptosis of cancer cells. In addition, GA inhibited the de novo lipogenesis of cancer cells through inducing activation of AMP-activated protein kinase (AMPK) signaling and downregulated the expression of key enzymes (e.g. acetyl-CoA carboxylase [ACC], fatty acid synthase [FASN]) involved in lipogenesis. Moreover, the in vivo experiment showed that GA reduced the expression of the key enzymes involved in lipogenesis and restrained the tumor growth. Taken together, our results suggest that GA may serve as a new candidate against tumor growth of pancreatic cancer partially through targeting pathway driving lipogenesis.
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