@article{Chen_Wu_Li_Zhu_Wang_Xu_Huang_Du_2019, title={Ginsenoside compound K inhibits growth of lung cancer cells via HIF-1α-mediated glucose metabolism}, volume={65}, url={https://cellmolbiol.org/index.php/CMB/article/view/2454}, DOI={10.14715/cmb/2019.65.4.8}, abstractNote={<p>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.</p>}, number={4}, journal={Cellular and Molecular Biology}, author={Chen, Hua-fei and Wu, Li-xin and Li, Xiao-feng and Zhu, You-cai and Wang, Wen-xian and Xu, Chun-wei and Huang, Zhang-zhou and Du, Kai-qi}, year={2019}, month={Apr.}, pages={48–52} }