烟酰胺腺嘌呤二核苷酸磷酸氧化酶 4 是通过甲状腺癌中糖酵解调节 mROS-HIF1α 轴的关键分子。
NADPH oxidase NOX4 is a glycolytic regulator through mROS-HIF1α axis in thyroid carcinomas.
机构信息
Otorhinolaryngology Head and Neck Surgery, The Third Hospital of Mianyang(Sichuan mental health center), No. 190 The East Jiannan Road, Mianyang, 621000, Sichuan, People's Republic of China.
Department of Clinical Laboratory, The Third Hospital of Mianyang(Sichuan mental health center), No. 190 The East Jiannan Road, Mianyang, 621000, Sichuan, People's Republic of China.
出版信息
Sci Rep. 2018 Oct 26;8(1):15897. doi: 10.1038/s41598-018-34154-8.
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 HIF1α decreasing glycolysis and retarded cell growth. These data suggests that Nox4 is potent oncotarget due to its role in regulating glycolysis through mROS-HIF1α pathway, thereby mediating proliferation in thyroid carcinomas.
NAD(P)H 氧化酶（NOX）家族成员 NOX4 的功能是生成活性氧（ROS），然而，NOX4 的分子功能尚未得到充分研究，有待阐明。为了阐明内源性 Nox4 在人甲状腺癌中的功能，使用乳头状甲状腺癌细胞研究通过敲低 NOX4 表达和敲除其功能伙伴 p22phox/CYBA 对细胞生长的影响。结果表明，由于缺氧时敲低 NOX4 和敲除 p22phox，线粒体 ROS（mROS）的增加被消除，从而使 HIF1α 不稳定，降低糖酵解并减缓细胞生长。这些数据表明，Nox4 是一种有效的致癌靶点，因为它通过 mROS-HIF1α 通路调节糖酵解，从而介导甲状腺癌的增殖。
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