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Nuclear envelope irregularity is induced by RET/PTC during interphase.

Andrew H Fischer1, Panya Taysavang, Sissy M Jhiang

  • 1Department of Pathology, Emory University Hospital, Atlanta, Georgia, USA. Fischa01@ummhc.org

The American Journal of Pathology
|August 26, 2003
PubMed
Summary
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Nuclear envelope irregularity in cancer may stem from abnormal re-assembly or interphase forces. RET/PTC1 oncogene, not RAS, causes this irregularity, suggesting it doesn't require postmitotic re-assembly.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Oncology

Background:

  • Nuclear envelope (NE) irregularity is a key cancer diagnostic marker.
  • The molecular mechanisms driving NE irregularity remain unclear.
  • Two hypotheses: abnormal postmitotic NE re-assembly or interphase dynamic forces.

Purpose of the Study:

  • To investigate the molecular basis of nuclear envelope irregularity induced by the RET/PTC1 oncogene.
  • To differentiate between abnormal NE re-assembly and interphase forces in causing NE irregularity.

Main Methods:

  • Microinjection of normal human thyroid epithelial cells with RET/PTC1, RET/PTC1 Deltazip, H-RAS, or dextran.
  • Fixation at 6 hours and 18-24 hours post-microinjection.
  • Immunofluorescence staining for lamins and microinjected products, followed by blind scoring of NE irregularity.

Related Experiment Videos

Main Results:

  • RET/PTC1 significantly increased NE irregularity (27% at 6h, 37% at 18-24h) compared to controls (6.5%).
  • RAS and dextran microinjections did not increase NE irregularity.
  • RET/PTC1 Deltazip induced significantly less NE irregularity than wild-type RET/PTC1.

Conclusions:

  • RET/PTC1 oncogene signaling is sufficient to induce nuclear envelope irregularity.
  • The rapid development of irregularity suggests it does not depend on postmitotic NE re-assembly.
  • Interphase dynamic forces likely play a role in RET/PTC1-induced NE irregularity.