TY - JOUR AU - Chen, Hua-fei AU - Wu, Li-xin AU - Li, Xiao-feng AU - Zhu, You-cai AU - Wang, Wen-xian AU - Xu, Chun-wei AU - Huang, Zhang-zhou AU - Du, Kai-qi PY - 2019/04/30 Y2 - 2024/03/29 TI - Ginsenoside compound K inhibits growth of lung cancer cells via HIF-1α-mediated glucose metabolism JF - Cellular and Molecular Biology JA - Cell Mol Biol (Noisy-le-grand) VL - 65 IS - 4 SE - Original Research Articles DO - 10.14715/cmb/2019.65.4.8 UR - https://cellmolbiol.org/index.php/CMB/article/view/2454 SP - 48-52 AB - <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> ER -