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Apoptosis in neural crest cells by functional loss of APC tumor suppressor gene

Sumitaka Hasegawa1, Tomoyuki Sato, Hiroshi Akazawa

  • 1Department of Cell Biology, The Cancer Institute, Japanese Foundation for Cancer Research, 1-37-1 Kami-Ikebukuro, Toshima-ku, Tokyo 170-8455, Japan.

Proceedings of the National Academy of Sciences of the United States of America
|January 5, 2002
PubMed

Insights

Inactivating the Apc gene causes cell death in neural crest cells, leading to birth defects. This contrasts with its role in colorectal cancer, where Apc loss promotes tumor growth.

Area of Science:

  • Developmental Biology
  • Cancer Biology
  • Genetics

Background:

  • The adenomatous polyposis coli (APC) gene is crucial in familial adenomatous polyposis coli (FAP) and colorectal cancer.
  • APC protein regulates beta-catenin, a key Wnt signaling pathway component.

Purpose of the Study:

  • To investigate the role of APC in neural crest development.
  • To understand the consequences of APC inactivation in neural crest cells.

Main Methods:

  • Conditional targeting of the Apc gene in mouse neural crest cells.
  • Analysis of apoptosis and developmental anomalies in embryos and neonates.

Main Results:

  • Apc inactivation in neural crest cells led to massive apoptosis around 11.5 days post coitum.
  • Apoptotic cells were observed in areas of beta-catenin accumulation.
  • Resulting craniofacial and cardiac anomalies were noted at birth.

Conclusions:

  • APC inactivation causes beta-catenin/Wnt signaling dysregulation leading to apoptosis in neural crest cells.
  • This contrasts with APC's role in colorectal cancer, highlighting tissue-specific functions.

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