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Mitochondrial DNA Integrity Is Maintained by APE1 in Carcinogen-Induced Colorectal Cancer.

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  • 1Department of Pharmacology and Toxicology, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico.

Molecular Cancer Research : MCR
|April 1, 2017
PubMed
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The base excision repair enzyme APE1 is crucial for maintaining mitochondrial DNA (mtDNA) integrity against damage from azoxymethane (AOM), a colorectal cancer carcinogen. Impaired APE1 function leads to increased nuclear DNA damage and tumor development.

Area of Science:

  • Mitochondrial biology
  • Cancer research
  • DNA repair mechanisms

Background:

  • Mitochondrial DNA (mtDNA) integrity alterations are observed in cancers, but their role in tumorigenesis is unclear.
  • The base excision repair (BER) enzyme APE1 plays a role in DNA repair.

Purpose of the Study:

  • To investigate the role of APE1 in protecting mtDNA from damage induced by azoxymethane (AOM), a colorectal cancer carcinogen.
  • To determine the impact of APE1 deficiency on AOM-induced colorectal tumorigenesis.

Main Methods:

  • Utilized a transgenic mouse model haploinsufficient for the apurinic/apyrimidinic endonuclease 1 (Apex1) gene.
  • Assessed mtDNA damage and repair kinetics using qPCR after AOM exposure.
  • Analyzed mtDNA and nuclear DNA lesions, mtDNA abundance, and tumor characteristics in wild-type (WT) and Apex1+/- mice.

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Main Results:

  • Apex1+/- mice exhibited slower repair kinetics and decreased mtDNA abundance following AOM exposure.
  • Both WT and Apex1+/- mice showed significant loss in mtDNA abundance in tumors.
  • Tumors from Apex1+/- mice displayed increased nuclear DNA lesions, higher proliferation, and abnormal histology, despite similar mtDNA lesions compared to WT.

Conclusions:

  • APE1 is essential for maintaining mtDNA integrity during AOM-induced colorectal cancer.
  • APE1 deficiency contributes to colorectal tumorigenesis through increased nuclear DNA damage and altered cellular proliferation.