ArticleCancers2026
Chromatin Engagement and Transcriptional Activity of the ZNF217 Exon 4-Skipping Isoform Are Associated with Breast Cancer Aggressiveness and Bone Metastasis.
Article in Cancers, 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
backgroundBreast cancer remains a major health issue, with bone metastases negatively impacting patient outcomes. The biochemical and biological functions of the exon 4-splice isoform (ZNF217-ΔE4) of the oncogenic transcription factor ZNF217 have been poorly investigated. METHODS/
resultsThis study, for the first time, elucidates through advanced live-cell single-molecule tracking microscopy that the C-terminus of ZNF217 influences chromatin engagement and binding stability. ZNF217-ΔE4 retains its ability to be recruited and to promote positive transcriptional activity. CRISPR/Cas9-mediated silencing of the ZNF217 gene in MDA-MB-231 breast cancer cells impairs cell aggressiveness, while reintroduction of the ZNF217-ΔE4 isoform is sufficient to restore increased cell proliferation, migration, invasion, and stemness features. In vivo, ZNF217 ΔE4-although less potent than the wild-type isoform-accelerates the formation of bone marrow micrometastases. A retrospective analysis of primary breast tumors revealed that patients with high
conclusionsOverall, this study identifies ZNF217-ΔE4 as a novel functional isoform that mediates breast cancer cell aggressiveness and bone marrow homing. It also highlights this isoform as a promising biomarker and potential therapeutic target for breast cancers at elevated risk of bone metastasis.
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