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Vol. 65 No. 4: Issue 4

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Ginsenoside compound K inhibits growth of lung cancer cells via HIF-1α-mediated glucose metabolism

https://doi.org/10.14715/cmb/2019.65.4.8
Hua-fei Chen
Department of Thoracic Disease Center, Zhejiang Rongjun Hospital, Jiaxing Zhejiang 314000, China
Li-xin Wu
Department of Thoracic Disease Center, Zhejiang Rongjun Hospital, Jiaxing Zhejiang 314000, China
Xiao-feng Li
Department of Thoracic Disease Center, Zhejiang Rongjun Hospital, Jiaxing Zhejiang 314000, China
You-cai Zhu
Department of Thoracic Disease Center, Zhejiang Rongjun Hospital, Jiaxing Zhejiang 314000, China
Wen-xian Wang
Department of Chemotherapy, Zhejiang Cancer Hospital, Hangzhou Zhejiang 310022, China
Chun-wei Xu
Department of Pathology, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital, Fuzhou Fujian 350014, China
Zhang-zhou Huang
Department of Medical Thoracic Oncology, Fujian Cancer Hospital, Fujian Medical University Cancer Hospital, Fuzhou Fujian 350014, China
Kai-qi Du
Department of Thoracic Disease Center, Zhejiang Rongjun Hospital, Jiaxing Zhejiang 314000, China

Corresponding Author(s) : Kai-qi Du

1141554200@qq.com

Cellular and Molecular Biology, Vol. 65 No. 4: Issue 4

Abstract

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths. Compound K, an active metabolite of ginsenosides, is reported to exhibit anti-cancer property in various types of human malignancies. The present study investigated the role of compound K on glucose metabolism in NSCLC cells and its underlying mechanism. Our study found that compound K dose-dependently inhibited the cell viability of NSCLC cells. Moreover, administration with compound K decreased glucose uptake and lactate secretion under normoxic and hypoxic conditions. Consistently, the expression of key enzymes (HK II, PDK1 and LDHA) involved in glucose metabolism were inhibited in compound K-treated tumor cells. In addition, compound K inhibited the expression of HIF-1α and its downstream gene GLUT1. On the contrary, overexpression of HIF-1α elevated metabolic reactions and partly attenuated the inhibitory role of compound K on NSCLC cell growth. These results demonstrate that compound K suppresses NSCLC cell growth via HIF-1α mediated metabolic alteration, contributing to novel anticancer therapy by targeting glucose metabolism.

Keywords

Non-small cell lung cancer Compound K HIF-1α Aerobic glycolysis.
Chen, H.- fei, Wu, L.- xin, Li, X.- feng, Zhu, Y.- cai, Wang, W.- xian, Xu, C.- wei, Huang, Z.- zhou, & Du, K.- qi. (2019). Ginsenoside compound K inhibits growth of lung cancer cells via HIF-1α-mediated glucose metabolism. Cellular and Molecular Biology, 65(4), 48–52. https://doi.org/10.14715/cmb/2019.65.4.8
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