ArticleCell reports2025
Hi-C profiling in tissues reveals 3D chromatin-regulated breast tumor heterogeneity informing a looping-mediated therapeutic avenue.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Alternative splicing rewires breast cancer and opens therapeutic avenues.Cell communication and signaling : CCS · 2026Review
- Article
- 3D chromatin architecture in cancer: mechanisms of dysregulation and emerging therapeutic strategies.Experimental & molecular medicine · 2026Review
- Connecting multiway enhancer-promoter interactions to changes in gene expression in cancer.bioRxiv : the preprint server for biology · 2026Article
- Cis-regulatory and long noncoding RNA alterations in breast cancer - current insights, biomarker utility, and the critical need for functional validation.Molecular oncology · 2026Review
- Pan-cancer 3D genomic analysis revealed extremely long Polycomb loops as the biomarker for sensitivity to Polycomb inhibition.bioRxiv : the preprint server for biology · 2025Article
- Review
- A 3D genome compendium of breast cancer progression.iScience · 2025Article
Corrections and comments
- Erratum issued
- Update of
Authors and funding
5 authors.
Funding
Abstract
The limitations of Hi-C (high-throughput chromosome conformation capture) profiling in in vitro cell culture include failing to recapitulate disease-specific physiological properties and lacking a clinically relevant disease microenvironment. In this study, we conduct Hi-C profiling in a pilot cohort of 12 breast tissues comprising two normal tissues, five ER+ breast primary tumors, and five tamoxifen-treated recurrent tumors. We demonstrate 3D chromatin-regulated breast tumor heterogeneity and identify a looping-mediated target gene, CA2, which might play a role in driving tamoxifen resistance. The inhibition of CA2 impedes tumor growth both in vitro and in vivo and reverses chromatin looping. The disruption of CA2 looping reduces tamoxifen-resistant cancer cell proliferation, decreases CA2 mRNA and protein expression, and weakens the looping interaction. Our study thus provides mechanistic and functional insights into the role of 3D chromatin architecture in regulating breast tumor heterogeneity and informs a new looping-mediated therapeutic avenue for treating breast cancer.
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