ArticleAgeing and cancer research & treatment2026
KCTD10 as a selective cancer dependency from transcription-replication conflicts (TRCs).
Article in Ageing and cancer research & treatment, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Transcription-replication conflicts (TRCs) are an increasingly recognized driver of genome instability in human cells. We recently identified the CUL3 adaptor KCTD10 as a sensor of co-directional TRCs, recruiting CUL3 to ubiquitinate transcriptional machinery and clear the path for replication forks. Here, we discuss the implications of this conflict-resolution pathway for human cancer. By integrating our mechanistic findings with large-scale functional genomics datasets, we identify oncogenic conditions that potentially create TRC-rich environments and render cells selectively dependent on KCTD10. These contexts reveal new mechanistic insights and potential therapeutic opportunities across a range of human cancers.
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