Induction of apoptosis and G2/M cell cycle arrest by DCC

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Updated: Oct 20, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Y Q Chen1, J T Hsieh, F Yao

  • 1Department of Pathology, Wayne State University, Detroit, Michigan 48201, USA.

Oncogene
|May 29, 1999
PubMed

Insights

The Deleted in Colorectal Cancer (DCC) gene product induces tumor cell death and cell cycle arrest. DCC

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The Deleted in Colorectal Cancer (DCC) gene encodes a cell surface receptor.
  • DCC gene inactivation is linked to human tumor progression.
  • The biological function of the DCC protein remains largely unknown.

Purpose of the Study:

  • To investigate the biological function of the DCC protein.
  • To elucidate the mechanisms by which DCC influences tumor cell behavior.

Main Methods:

  • Studied the effects of DCC expression on tumor cell lines.
  • Assessed caspase-3 activation and programmed cell death (apoptosis).
  • Analyzed cell cycle progression and Cdk1 activity.

Main Results:

  • DCC expression triggered caspase-3 activation and apoptosis in tumor cells.
  • Apoptosis was observed within 24 hours, coinciding with PARP cleavage.
  • DCC expression induced G2/M cell cycle arrest by inhibiting Cdk1 activity.
  • The apoptosis inhibitory gene Bcl-2 could not prevent DCC-induced apoptosis.

Conclusions:

  • DCC protein may signal for caspase activation or Cdk1 inhibition.
  • These findings suggest a mechanism for DCC's tumor-suppressive function.

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