Chromatin interaction analysis reveals changes in small chromosome and telomere clustering between epithelial and breast cancer cells
Open accessAbstract
BACKGROUND: Higher-order chromatin structure is often perturbed in cancer and other pathological states. Although several genetic and epigenetic differences have been charted between normal and breast cancer tissues, changes in higher-order chromatin organization during tumorigenesis have not been fully explored. To probe the differences in higher-order chromatin structure between mammary epithelial and breast cancer cells, we performed Hi-C analysis on MCF-10A mammary epithelial and MCF-7 breast cancer cell lines. RESULTS: Our studies reveal that the small, gene-rich chromosomes chr16 through chr22 in the MCF-7 breast cancer genome display decreased interaction frequency with each other compared to the inter-chromosomal interaction frequency in the MCF-10A epithelial cells. Interestingly, this finding is associated with a higher occurrence of open compartments on chr16-22 in MCF-7 cells. Pathway analysis of the MCF-7 up-regulated genes located in altered compartment regions on chr16-22 reveals pathways related to repression of WNT signaling. There are also differences in intra-chromosomal interactions between the cell lines; telomeric and sub-telomeric regions in the MCF-10A cells display more frequent interactions than are observed in the MCF-7 cells. CONCLUSIONS: We show evidence of an intricate relationship between chromosomal organization and gene expression between epithelial and breast cancer cells. Importantly, this work provides a genome-wide view of higher-order chromatin dynamics and a resource for studying higher-order chromatin interactions in two cell lines commonly used to study the progression of breast cancer.
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There was a high overlap (85% for K562 and 83.4% for MCF7) between the common boundaries and TAD boundaries found in cancer cell lines.
“We observed a high overlap with boundaries from a leukemia cell line K562 (ref. 17) and a breast cancer cell line MCF7 (ref. 20) (85% and 83.4%, respectively; Extended Data Fig. 1f,g).”
From Disruption of chromatin folding domains by somatic genomic rearrangements in human cancer (2020) · cites this paper as [20]
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- Authors
- Barutcu, A. R., Lajoie, B. R., McCord, R. P., Tye, C. E., Hong, D., Messier, T. L., Browne, G., van Wijnen, A. J., Lian, J. B., Stein, J. L., Dekker, J., Imbalzano, A. N., & Stein, G. S.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- University of Vermont (US)
- Corresponding author
- Stein, Gary S.
- ORCID
- Venue
- Genome Biology
- Published
- 2015-09-28
- Volume
- 16
- Issue
- 1
- Pages
- 214-214
- ISSN
- 1465-6906 (ISSN-L)
- 1474-760X
- PMC
- PMC4587679
- OpenAlex
- W2156988725
- Cited by
- 250
- References
- 73
- Citations by year
- 2026: 13 · 2025: 19 · 2024: 21 · 2023: 25 · 2022: 24 · 2021: 41 · 2020: 26 · 2019: 19 · 2018: 24 · 2017: 16 · 2016: 17 · 2015: 1 · 2014: 2
- FWCI
- 8.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Genome biology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship@UMassChan (submittedVersion, cc-by)
- Funders
- National Cancer Institute (P01 CA082834)
- Pfizer Investigator-Initiated Research Award - IIR Grant (WS2049100)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Keywords
- higher-order chromatin structure, small chromosomes, MCF-7 cells, chromatin compartments, gene expression regulation, carcinogenesis, Hi-C
- MeSH terms
- Breast Neoplasms, Chromatin, Epithelial Cells, Female, Humans, Gene Expression Regulation, Neoplastic, Telomere, Mammary Glands, Human, Epigenesis, Genetic, MCF-7 Cells, Carcinogenesis
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