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Tumor progression in Apc(1638N) mice with Exo1 and Fen1 deficiencies

M Kucherlapati1, A Nguyen, M Kuraguchi

  • 1Harvard-Partners Center for Genetics and Genomics, Harvard Medical School, Boston, MA 02115, USA. mkucherlapati@rics.bwh.harvard.edu

Oncogene
|April 25, 2007
PubMed

Insights

Exonuclease 1 (Exo1) shows a modest tumor suppressor function in early gastrointestinal cancer. While it increases tumor incidence with Apc mutations, it also enhances immune response, preventing early tumor progression.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • Flap endonuclease 1 (Fen1) and exonuclease 1 (Exo1) share sequence homology and nuclease functions.
  • Both enzymes are involved in DNA metabolism but have distinct roles.
  • Fen1 promotes tumor progression when combined with Apc(1638N).

Purpose of the Study:

  • To investigate Exo1's role as a modifier of Apc(1638N) in tumorigenesis.
  • To explore Exo1's potential function in DNA mismatch repair (MMR) pathways.
  • To understand Exo1's impact on gastrointestinal (GI) tumor development and progression.

Main Methods:

  • Analysis of genetically modified mice with combined Apc(1638N) and Exo1 mutations.
  • Assessment of tumor incidence, multiplicity, and progression in Apc(1638N) Exo1 and Apc(1638N) Exo1 Fen1 models.
  • Evaluation of survival rates and immune response in the studied mouse models.

Main Results:

  • Combined Apc(1638N) and Exo1 mutations led to moderate increases in tumor incidence and multiplicity.
  • Apc(1638N) Exo1 mice exhibited decreased survival due to infections from impaired immune response.
  • Apc(1638N) Exo1 Fen1 mice survived longer and died from invasive GI tumors with microsatellite instability (MSI).

Conclusions:

  • Exo1 demonstrates a modest tumor suppressor function in early GI tumorigenesis.
  • Exo1 influences immune response, impacting survival in Apc-mutant mice.
  • The interplay between Exo1, Fen1, and Apc affects tumor progression and host survival.

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