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Dozmorov, Mikhail G; Marshall, Maggie A; Rashid, Narmeen S; Grible, Jacqueline M; Valentine, Aaron; Olex, Amy L; Murthy, Kavita; Chakraborty, Abhijit; Reyna, Joaquin; Figueroa, Daniela Salgado; Hinojosa-Gonzalez, Laura; Da-Inn Lee, Erika; Baur, Brittany A; Roy, Sushmita; Ay, Ferhat; Harrell, J Chuck
Scientific reports, 04/2023, Volume: 13, Issue: 1Journal Article
Changes in the three-dimensional (3D) structure of the genome are an emerging hallmark of cancer. Cancer-associated copy number variants and single nucleotide polymorphisms promote rewiring of chromatin loops, disruption of topologically associating domains (TADs), active/inactive chromatin state switching, leading to oncogene expression and silencing of tumor suppressors. However, little is known about 3D changes during cancer progression to a chemotherapy-resistant state. We integrated chromatin conformation capture (Hi-C), RNA-seq, and whole-genome sequencing obtained from triple-negative breast cancer patient-derived xenograft primary tumors (UCD52) and carboplatin-resistant samples and found increased short-range (< 2 Mb) interactions, chromatin looping, formation of TAD, chromatin state switching into a more active state, and amplification of ATP-binding cassette transporters. Transcriptome changes suggested the role of long-noncoding RNAs in carboplatin resistance. Rewiring of the 3D genome was associated with TP53, TP63, BATF, FOS-JUN family of transcription factors and led to activation of aggressiveness-, metastasis- and other cancer-related pathways. Integrative analysis highlighted increased ribosome biogenesis and oxidative phosphorylation, suggesting the role of mitochondrial energy metabolism. Our results suggest that 3D genome remodeling may be a key mechanism underlying carboplatin resistance.
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