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Updated: Aug 11, 2026

Characterization of Molecular Mechanisms of In vivo UVR Induced Cataract
13:56

Characterization of Molecular Mechanisms of In vivo UVR Induced Cataract

Published on: November 28, 2012

Role for cyclin D1 in UVC-induced and p53-mediated apoptosis

H Hiyama1, S A Reeves

  • 1Molecular Neuro-Oncology, Neuroscience Center, Neurosurgical Services, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA.

Cell Death and Differentiation
|June 25, 1999
PubMed

Insights

Cyclin D1 abrogates UV-induced G1 arrest and is essential for cell cycle re-entry and p53-mediated apoptosis in glioblastoma cells. This finding reveals a critical role for cyclin D1 in DNA damage response pathways.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • DNA damaging agents like UV radiation trigger cell cycle arrest and apoptosis.
  • Glioblastoma cells exhibit complex responses to DNA damage, involving cell cycle regulation and programmed cell death.

Purpose of the Study:

  • To investigate the role of cyclin D1 in UV-induced cell cycle arrest and apoptosis in human U343 glioblastoma cells.
  • To determine if cyclin D1 levels influence p53-mediated apoptosis following DNA damage.

Main Methods:

  • Analysis of cyclin D1, cdk4, p53, and p21 protein levels in UV-irradiated U343 cells.
  • Examination of cyclin D1/cdk4 complex formation during cell cycle progression.
  • Utilizing U343 cells engineered to ectopically express cyclin D1 to assess its functional impact.

Main Results:

  • UV irradiation caused G1 arrest with decreased cyclin D1/cdk4 complexes and increased p53/p21 levels.
  • Apoptosis occurred after cell cycle re-entry, coinciding with cyclin D1/cdk4 complex reappearance.
  • Ectopic cyclin D1 expression overcame UV-induced G1 arrest, and apoptosis induction was dependent on cyclin D1 levels.

Conclusions:

  • Cyclin D1 plays a crucial role in overcoming UV-induced G1 arrest, enabling cell cycle re-entry.
  • The p53-mediated apoptotic response to DNA damage is modulated by cyclin D1 levels.
  • Cyclin D1 expression is essential for both cell cycle re-entry and subsequent apoptosis following DNA damage in glioblastoma cells.

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