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NDRG2 acts as a PERK co-factor to facilitate PERK branch and ERS-induced cell death

Mei Zhang1, Xiping Liu1,2, Qinhao Wang1

  • 1State Key Laboratory of Cancer Biology, Department of Biochemistry and Molecular Biology, The Fourth Military Medical University, Xi'an, China.

FEBS Letters
|September 27, 2017
PubMed

Insights

NDRG2 is a tumor suppressor that responds to stress. It acts as a co-factor for the PERK pathway, enhancing endoplasmic reticulum stress-induced apoptosis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • NDRG2 (Ndrg family member 2) is a stress-responsive tumor suppressor.
  • Its role in endoplasmic reticulum stress (ERS) response is not well understood.

Discussion:

  • NDRG2 expression is upregulated by ERS inducers like Tg, Tm, and DTT in hepatoma cells.
  • NDRG2 interacts with PERK (protein kinase RNA-like ER kinase), a key component of the unfolded protein response.
  • This interaction enhances PERK pathway signaling, specifically activating downstream ATF4 and CHOP.

Key Insights:

  • NDRG2 acts as a co-factor for the PERK pathway during ERS.
  • NDRG2 facilitates ERS-induced apoptosis, partly mediated by ATF4 and CHOP.
  • This highlights NDRG2's novel role in cellular stress response and cancer biology.

Outlook:

  • Further investigation into NDRG2's precise co-factor mechanism.
  • Exploring therapeutic strategies targeting the NDRG2-PERK axis in cancer.
Keywords:
PERKUPRApoptosisER stressNDRG2

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