ArticleiScience2026
CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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3 authors.
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Abstract
CTCF/cohesin-binding sites (CBSs) at the chromatin-loop anchors and topologically associating domains are frequently mutated in cancer; however, the underlying molecular mechanisms remain unclear. Here, we investigate whether CTCF and cohesin co-binding on DNA imposes constraints on DNA replication, leading to DNA damage and genomic instability. Our results reveal that CTCF and cohesin remain co-bound to DNA during replication in cancer cells (HeLa). Furthermore, analysis of DNA damage response/repair (DDR) proteins-including MRE11, STN1, γH2AX, and RAD51-showed a high enrichment of these proteins at CBSs, compared with immediate flanking regions. The loss of DDR genes in tumor genomes showed a significant enrichment of somatic mutations at CBSs compared with those tumors with intact DDR genes. Together, we propose that CTCF and cohesin co-binding can impede replication fork progression, leading to DNA damage and DDR activation. However, in cells with defective DDR, these lesions may promote genomic instability at CBSs.
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