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Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
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Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

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NRF2-regulated cell cycle arrest at early stage of oxidative stress response mechanism

Margita Márton1, Nikolett Tihanyi1, Pál Gyulavári2

  • 1Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Hungary.

Plos One
|November 29, 2018
PubMed

Insights

Nuclear factor erythroid 2-related factor 2 (NRF2) plays a crucial role in blocking cell division during oxidative stress. NRF2, alongside the PERK pathway, inhibits Cyclin D1 activity, leading to cell cycle arrest.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Oxidative stress activates signaling pathways, including those involving PERK and NRF2.
  • Cell division must be halted during oxidative stress.
  • The PERK pathway down-regulates Cyclin D1, causing cell cycle arrest, but NRF2's role is unclear.

Purpose of the Study:

  • To investigate the interaction between NRF2 and cell cycle regulators under oxidative stress.
  • To elucidate the role of NRF2 in the cell cycle response to oxidative damage.

Main Methods:

  • Utilized molecular biological techniques to study oxidative stress responses.
  • Examined the effect of oxidative agents on Cyclin D1 levels and activity.
  • Investigated the impact of PERK and NRF2 silencing on cell cycle inhibitors.

Main Results:

  • Cyclin D1 levels remained stable, but its activity was inhibited by stoichiometric inhibitors (p15, p21, p27) during low-level oxidative stress.
  • The inhibitory effect on Cyclin D1 was abolished upon silencing of PERK or NRF2.
  • NRF2 is confirmed to be essential for blocking Cyclin D1 activity via inhibitors during early oxidative stress.

Conclusions:

  • NRF2 is a key mediator in the cell cycle arrest response to oxidative stress.
  • NRF2 collaborates with the PERK pathway to regulate Cyclin D1 activity and cell division.
  • Findings reveal a novel crosstalk between NRF2 and cell cycle machinery under oxidative stress.

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