ArticleProceedings of the National Academy of Sciences of the United States of America2025
Cancer cells subvert the primate-specific KRAB zinc finger protein ZNF93 to control APOBEC3B.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Review
- Identification of a lipid oxygen radical defense pathway and its epigenetic control.Nature communications · 2025Article
- Cancer cells subvert the primate-specific KRAB zinc finger protein ZNF93 to control APOBEC3B.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
ZNF93 is a primate-restricted Krüppel-associated box zinc finger protein responsible for repressing 20- to 12-My-old L1 transposable elements. Here, we reveal that ZNF93 also regulates the key cancer driver APOBEC3B-a mutagenic enzyme linked to tumorigenesis and cancer progression. ZNF93 depletion impairs DNA synthesis, activates replication and DNA damage checkpoints, and triggers proinflammatory phenotypes. Conversely, its overexpression enhances resistance to exogenous genotoxic stress, mirroring the effects observed with APOBEC3B depletion. ZNF93 expression correlates with cell proliferation rates and is overexpressed in many cancer types. These findings suggest that ZNF93 serves as a critical guardian of genome integrity, co-opted by cancer cells to counterbalance APOBEC3B-induced and L1-derived genomic instability and inflammation.
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