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An Enzyme that Defends Against Viruses Could Double Cancer Mutations
An enzyme that protects human cells against rotaviruses, such as HIV, can help drive cancer evolution towards greater malignancy, according to a study led by investigators at Weill Cornell Medicine. Scientists believed that the enzyme might be a potential target for future cancer treatments.
The journal Cancer Research published the novel findings in December 2022.
Related Article: Repairing Genetic Mutations in Neurological Diseases with RNA Targeting Strategy
The Virus-Protecting Enzyme As a Double-Edged Sword
The APOBEC3 family of enzymes is capable of mutating RNA or DNA, by chemically modifying a cytosine nucleotide in the genetic code. Its capability of causing mutation in the viral genome is originally thought to aid in fighting retroviruses, by interrupting viral replication.
However, these cellular mutations can create long-lasting alterations in the human genetic code, introducing errors even after the virus is gone. Thus, the hypothesis that these enzymes could promote cancer formation started nearly a decade ago. Thanks to the advancement in DNA-sequencing techniques, biologists can have a more in-depth look into events happening in cancer cells at a genetic level.
APOBEC3G Increased the Risk of Developing Bladder Cancer
APOBEC3G is a human enzyme that is not found in mice. Hence, the team started by knocking out the sole APOBEC3-type enzyme in mice and replaced it with the human APOBEC3G gene. Mice were then exposed to a bladder cancer-promoting chemical that is similar to the ones found in cigarette smoke.
As a result, mice with the APOBEC3G gene were 76 percent more likely to develop bladder cancer compared to the 53 percent of mice who had their APOBEC gene knocked out but not replaced. What’s more, all the knockout-only mice survived after a 30-week observation period, whereas nearly one-third of the APOBEC3G mice died of cancer.
The reason behind the huge difference in mortality rates is that APOBEC3G mice showed twice as many mutations compared to the tumors in knockout-only mice. The great mutational burden and genomic diversity in the tumors accounted for the greater malignancy and mortality in the APOBEC3G mice.
Last but not least, the researchers aimed to prove the connections of APOBEC3G’s mutational signature in human bladder cancer using a widely used tumor DNA database, which is The Cancer Genome Atlas, and discovered that these mutations appear to be common in bladder cancers, and are related to worse outcomes.
To sum up, the study dissects the mutagenic impact of APOBEC3G on the bladder cancer genome, identifying it contributes to genomic instability, and tumor mutational burden, while also providing new insight into using APOBEC3G as a new target in precision medicine.
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