NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas

被引：33
|
作者：
Tang, Ping [1 ]
Dang, Hao [2 ]
Huang, Jie [3 ]
Xu, Tao [1 ]
Yuan, Ping [1 ]
Hu, Jun [1 ]
Sheng, Jian-feng [1 ]
机构：
[1] Third Hosp Mianyang, Sichuan Mental Hlth Ctr, Otorhinolaryngol Head & Neck Surg, 190 East Jiannan Rd, Mianyang 621000, Sichuan, Peoples R China
[2] Third Hosp Mianyang, Sichuan Mental Hlth Ctr, Dept Clin Lab, 190 East Jiannan Rd, Mianyang 621000, Sichuan, Peoples R China
[3] Yunnan Jiehui Biotech Ltd, 9 Daxi Rd, Kunming 650215, Yunnan, Peoples R China
来源：
SCIENTIFIC REPORTS | 2018年 / 8卷
关键词：
RENAL TUMORIGENESIS; HYPOXIA; EXPRESSION;
D O I：
10.1038/s41598-018-34154-8
中图分类号：
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
The function of the NAD(P)H oxidases (NOXs) family member NOX4 is to generate reactive oxygen species (ROS), however, the molecular function of NOX4 has not been fully studied and waiting to be clarified. To elucidate the function of endogenous Nox4 in human thyroid carcinomas, papillomatosis thyroid cancer cells were used to study the cell growth by knocking down the expression of NOX4 and knocking out its functional partner p22phox/CYBA. As a result, the increasement of mitochondrial ROS(mROS) was abolished due to both knockdown of NOX4 and p22phox knockout in hypoxia, which destabilized HIF1 alpha. decreasing glycolysis and retarded cell growth. These data suggests that Nox4 is potent oncotarget due to its role in regulating glycolysis through mROS-HIF1 alpha pathway, thereby mediating proliferation in thyroid carcinomas.
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页数：9
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