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Updated: Jun 5, 2025

In Vitro Ubiquitination and Deubiquitination Assays of Nucleosomal Histones
Published on: July 25, 2019
An overview of the functions and mechanisms of APOBEC3A in tumorigenesis
Yuqi Yang1,2, Nan Liu1,2, Likun Gong1,2
1State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
Abstract:
The APOBEC3 (A3) family plays a pivotal role in the immune system by performing DNA/RNA single-strand deamination. Cancers mostly arise from the accumulation of chronic mutations in somatic cells, and recent research has highlighted the A3 family as a major contributor to tumor-associated mutations, with A3A being a key driver gene leading to cancer-related mutations. A3A helps to defend the host against virus-induced tumors by editing the genome of cancer-associated viruses that invade the host. However, when it is abnormally expressed, it leads to persistent, chronic mutations in the genome, thereby fueling tumorigenesis. Notably, A3A is prominently expressed in innate immune cells, particularly macrophages, thereby affecting the functional state of tumor-infiltrating immune cells and tumor growth. Furthermore, the expression of A3A in tumor cells may directly affect their proliferation and migration. A growing body of research has unveiled that A3A is closely related to various cancers, which signifies the potential significance of A3A in cancer therapy. This paper mainly classifies and summarizes the evidence of the relationship between A3A and tumorigenesis based on the potential mechanisms, aiming to provide valuable references for further research on the functions of A3A and its development in the area of cancer therapy.
Insights
The APOBEC3A (A3A) enzyme, crucial for immunity, can drive cancer mutations when abnormally expressed. Understanding A3A
Area of Science:
- Immunology
- Genetics
- Oncology
Background:
- The APOBEC3 (A3) gene family is vital for innate immunity, involved in DNA/RNA single-strand deamination.
- Aberrant expression of A3A is increasingly recognized as a significant contributor to tumor-associated mutations and tumorigenesis.
- A3A's role in editing viral genomes contrasts with its potential to induce chronic mutations in host genomes.
Purpose of the Study:
- To comprehensively review and categorize the evidence linking A3A to cancer development.
- To elucidate the underlying mechanisms through which A3A influences tumorigenesis.
- To highlight A3A's potential as a therapeutic target in cancer treatment.
Main Methods:
- Literature review and synthesis of existing research on A3A and cancer.
- Classification of studies based on proposed mechanisms of A3A-driven tumorigenesis.
- Analysis of A3A expression patterns in various cancer types and immune cells.
Main Results:
- A3A acts as a key driver gene in cancer-related mutations, contributing to somatic cell mutations.
- Abnormal A3A expression in tumor cells can directly impact proliferation and migration.
- A3A expression in macrophages influences tumor-infiltrating immune cells and tumor growth.
Conclusions:
- A3A is closely implicated in the development of diverse cancers.
- Targeting A3A presents a promising avenue for novel cancer therapies.
- Further research into A3A's functions is crucial for advancing cancer treatment strategies.
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