Open AccessApolipoprotein B mRNA editing enzyme catalytic polypeptide‐like family genes activation and regulation during tumorigenesis
Author(s) -
Gao Jianlong,
Choudhry Hani,
Cao Wei
Publication year - 2018
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13658
Subject(s) - apobec , carcinogenesis , biology , cytidine deaminase , apobec3g , genetics , somatic hypermutation , epigenomics , retrotransposon , genome instability , transmethylation , mutagenesis , cytosine deaminase , rna editing , gene , mutation , genome , gene expression , dna methylation , dna , dna damage , b cell , methylation , antibody , genetic enhancement , transposable element
Cancer is currently viewed as a disease of evolving genomic instability and abnormal epigenomic modifications. Most solid cancers harbor oncogenic gene mutations driven by both extrinsic and intrinsic factors. Apolipoprotein B mRNA editing catalytic polypeptide‐like family ( APOBEC ) enzymes have an intrinsic deamination activity to convert cytosine to uracil during RNA editing and retrovirus or retrotransposon restriction. Beyond their natural defense in innate immunity, compelling evidence showed that a subclass of APOBEC 3 can cause high mutation burden in various types of cancer genomes, and high expression subtypes of APOBEC 3 may contribute to drug resistance and associate with clinical outcomes. The underlying molecular mechanisms of APOBEC ‐mediated hypermutation phenotype are poorly understood. In this review, we discuss the linkage of activation‐induced deaminase ( AID )/ APOBEC 3 enzymes to tumorigenesis, highlight the dysregulatory mechanisms of APOBEC 3 activities during cancer development, and propose potential approaches to targeting APOBEC 3‐mediated mutagenesis for cancer interventions.