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APOBEC-Induced Mutagenesis in Cancer
Tony M Mertz1, Christopher D Collins1, Madeline Dennis1
1School of Molecular Biosciences and Center for Reproductive Biology, Washington State University, Pullman, Washington, USA;
Annual Review of Genetics
|August 26, 2022
Summary
Dysregulated APOBEC enzymes accelerate cancer by causing mutations. Understanding these cancer mutation signatures is key to developing effective, long-lasting cancer therapeutics.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Cancer development, progression, and relapse are often driven by somatic cell mutations.
- Elevated mutation rates accelerate carcinogenesis and impede therapeutic development.
- Mutation signatures in human cancer genomes reveal specific endogenous and environmental mutational processes.
Purpose of the Study:
- To review the current understanding of apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) roles in cancer mutagenesis.
- To discuss the impact of APOBECs on cancer progression, metastasis, and therapeutic resistance.
- To explore biological factors influencing APOBEC mutagenic capacity.
Main Methods:
- Review of recent human cancer genome sequencing data.
- Analysis of mutation signatures associated with specific mutational processes.
- Examination of APOBEC enzyme activity and its consequences on DNA.
Main Results:
- APOBEC dysregulation is a frequent cause of observed mutation signatures in human cancers.
- APOBEC-mediated deamination of cytidines leads to C-to-T and C-to-G substitutions.
- APOBEC-generated genetic heterogeneity fuels cancer development, metastasis, and treatment resistance.
Conclusions:
- APOBECs play a significant role in cancer mutagenesis.
- Understanding APOBEC activity is crucial for developing targeted cancer therapies.
- Further research into biological regulators of APOBECs may reveal new therapeutic strategies.
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