TY - JOUR
T1 - Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis
AU - Ma, Jiguang
AU - Duan, Wanxing
AU - Han, Suxia
AU - Lei, Jianjun
AU - Xu, Qinhong
AU - Chen, Xin
AU - Jiang, Zhengdong
AU - Nan, Ligang
AU - Li, Jiahui
AU - Chen, Ke
AU - Han, Liang
AU - Wang, Zheng
AU - Li, Xuqi
AU - Wu, Erxi
AU - Huo, Xiongwei
PY - 2015
Y1 - 2015
N2 - 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 AMPactivated 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.
AB - 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 AMPactivated 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.
KW - AMP-activated protein kinase (AMPK)
KW - Cancer metabolism
KW - Ginkgolic acid (GA)
KW - Lipogenesis
KW - Pancreatic cancer
UR - https://www.scopus.com/pages/publications/84940755897
U2 - 10.18632/oncotarget.3663
DO - 10.18632/oncotarget.3663
M3 - 文章
C2 - 25895130
AN - SCOPUS:84940755897
SN - 1949-2553
VL - 6
SP - 20993
EP - 21003
JO - Oncotarget
JF - Oncotarget
IS - 25
ER -