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miR-216b regulation of c-Jun mediates GADD153/CHOP-dependent apoptosis

Zhenhua Xu1, Yiwen Bu1, Nilesh Chitnis1

  • 1Department of Biochemistry, Hollings Cancer Center, Medical University of South Carolina, 86 Jonathan Lucas Street, 3400, Charleston, South Carolina 29425, USA.

Nature Communications
|May 14, 2016
PubMed

Insights

The unfolded protein response (UPR) regulates cell homeostasis. This study shows micro-RNA 216b (miR-216b) mediates CHOP/GADD153-dependent apoptosis by targeting c-Jun during ER stress.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • The unfolded protein response (UPR) is crucial for maintaining cellular homeostasis.
  • CHOP/GADD153 is a key transcription factor involved in UPR-mediated apoptosis, but its precise regulatory mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which CHOP/GADD153 regulates apoptosis during ER stress.
  • To identify downstream targets of CHOP/GADD153 involved in cell death pathways.

Main Methods:

  • Investigated the role of micro-RNA 216b (miR-216b) in CHOP/GADD153-dependent apoptosis.
  • Utilized PERK and Ire1 signaling pathways manipulation.
  • Analyzed the direct targeting of c-Jun by miR-216b.

Main Results:

  • CHOP/GADD153 directly regulates the expression of miR-216b.
  • MiR-216b accumulation is dependent on PERK signaling and antagonized by Ire1.
  • MiR-216b directly targets c-Jun, reducing AP-1-dependent transcription and sensitizing cells to apoptosis.

Conclusions:

  • MiR-216b acts as a critical mediator of CHOP/GADD153-induced apoptosis.
  • The convergence of PERK and Ire1 signaling pathways regulates miR-216b levels.
  • These findings provide novel insights into the molecular control of ER stress-induced cell death.

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