糖酵解
细胞生长
失巢
癌症研究
己糖激酶
厌氧糖酵解
调解人
代谢组学
A549电池
化学
细胞生物学
生物
细胞凋亡
生物化学
酶
程序性细胞死亡
生物信息学
作者
Xuefang Cheng,Fang Liu,Huiying Liu,Guangji Wang,Haiping Hao
标识
DOI:10.1016/j.bbrc.2017.12.160
摘要
NAD(P)H:quinone oxidoreductase 1 (NQO1), a cytoplasmic 2-electron reductase, has been considered as a potential poor prognostic biomarker and a promising therapeutic target for patients with non-small cell lung cancer (NSCLC) due to its frequent overexpression and significantly increased activity in NSCLC. Previous studies have shown that depleting tumor-NQO1 potentiates anoikis and inhibits growth of NSCLC. However, the underlying mechanisms whereby NQO1 potentiates proliferation have not been fully understood. In this study, based on a metabolomics analysis, we found that cell proliferation inhibition upon NQO1 depletion was accompanied by suppressed glycometabolism in NQO1 high expression human NSCLC A549 cells. Also we found that NQO1 depletion significantly decreased the gene expression levels of hexokinase II (HKII), a key mediator of aerobic glycolysis responsible for the transformation of glucose into glucose-6-phosphate. Taken together, we proposed that NQO1 could potentiate NSCLC cell proliferation by enhancing cellular glycometabolism, and HKII is a key mediator of this mechanism.
科研通智能强力驱动
Strongly Powered by AbleSci AI