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

Ping Tang1, Hao Dang2, Jie Huang3

  • 1Otorhinolaryngology 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.

Scientific Reports
|October 28, 2018
PubMed

Insights

NOX4 generates reactive oxygen species (ROS) in thyroid cancer. Inhibiting NOX4 reduces mitochondrial ROS, hindering cancer cell growth by impacting the HIF1α-glycolysis pathway.

Area of Science:

  • Biochemistry
  • Oncology
  • Cell Biology

Background:

  • NAD(P)H oxidases (NOXs) generate reactive oxygen species (ROS).
  • The specific molecular functions of NOX4 remain incompletely understood.
  • NOX4's role in human thyroid carcinomas requires further elucidation.

Purpose of the Study:

  • To investigate the function of endogenous NOX4 in human thyroid carcinomas.
  • To analyze the impact of NOX4 and its partner p22phox/CYBA on thyroid cancer cell proliferation.
  • To clarify the molecular mechanisms underlying NOX4's function in this cancer type.

Main Methods:

  • Utilized papillomatosis thyroid cancer cells.
  • Performed gene knockdown of NOX4.
  • Conducted knockout of the functional partner p22phox/CYBA.
  • Assessed mitochondrial ROS (mROS) levels under hypoxic conditions.
  • Evaluated the stability of HIF1α and glycolysis rates.
  • Monitored cancer cell growth.

Main Results:

  • Knockdown of NOX4 and knockout of p22phox abolished the increase in mitochondrial ROS (mROS) under hypoxia.
  • This reduction in mROS led to destabilization of HIF1α.
  • Destabilized HIF1α resulted in decreased glycolysis.
  • The observed changes in glycolysis and HIF1α significantly retarded cancer cell growth.

Conclusions:

  • NOX4 plays a critical role in regulating glycolysis via the mROS-HIF1α pathway in thyroid carcinomas.
  • NOX4 is a potential oncotarget for therapeutic intervention in thyroid cancer.
  • Targeting NOX4 may offer a strategy to inhibit cancer cell proliferation by disrupting glycolysis.

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