Chromatin interaction analysis reveals changes in small chromosome and telomere clustering between epithelial and breast cancer cells
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 explore...
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creator | Barutcu, A Rasim Lajoie, Bryan R McCord, Rachel P Tye, Coralee E Hong, Deli Messier, Terri L Browne, Gillian van Wijnen, Andre J Lian, Jane B Stein, Janet L Dekker, Job Imbalzano, Anthony N Stein, Gary S |
description | 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.
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.
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. |
doi_str_mv | 10.1186/s13059-015-0768-0 |
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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.
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.</description><identifier>ISSN: 1474-760X</identifier><identifier>ISSN: 1474-7596</identifier><identifier>EISSN: 1474-760X</identifier><identifier>DOI: 10.1186/s13059-015-0768-0</identifier><identifier>PMID: 26415882</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Bioinformatics ; Breast cancer ; breast neoplasms ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cancer ; Cancer cells ; Carcinogenesis ; Chromatin ; Chromatin - genetics ; Chromosomes ; Comparative analysis ; Development and progression ; Discovery tools ; Epigenesis, Genetic ; Epigenetic inheritance ; epigenetics ; Epithelial cells ; Epithelial Cells - metabolism ; Epithelial Cells - pathology ; epithelium ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Genetic aspects ; Genetic research ; genome ; Genomes ; Genomics ; Humans ; Mammary Glands, Human - metabolism ; Mammary Glands, Human - pathology ; MCF-7 Cells ; Morphology ; neoplasm cells ; Patient outcomes ; Stem cells ; Telomere - genetics ; Telomeres ; Tumor cell lines ; Tumorigenesis ; Wnt protein</subject><ispartof>Genome Biology, 2015-09, Vol.16 (1), p.214-214, Article 214</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>2015. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Barutcu et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c661t-45854b7718388143d20847ca1492c4036dceb71d0cfdfc671ff9f17cdfd8fa263</citedby><cites>FETCH-LOGICAL-c661t-45854b7718388143d20847ca1492c4036dceb71d0cfdfc671ff9f17cdfd8fa263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587679/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4587679/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26415882$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Barutcu, A Rasim</creatorcontrib><creatorcontrib>Lajoie, Bryan R</creatorcontrib><creatorcontrib>McCord, Rachel P</creatorcontrib><creatorcontrib>Tye, Coralee E</creatorcontrib><creatorcontrib>Hong, Deli</creatorcontrib><creatorcontrib>Messier, Terri L</creatorcontrib><creatorcontrib>Browne, Gillian</creatorcontrib><creatorcontrib>van Wijnen, Andre J</creatorcontrib><creatorcontrib>Lian, Jane B</creatorcontrib><creatorcontrib>Stein, Janet L</creatorcontrib><creatorcontrib>Dekker, Job</creatorcontrib><creatorcontrib>Imbalzano, Anthony N</creatorcontrib><creatorcontrib>Stein, Gary S</creatorcontrib><title>Chromatin interaction analysis reveals changes in small chromosome and telomere clustering between epithelial and breast cancer cells</title><title>Genome Biology</title><addtitle>Genome Biol</addtitle><description>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.
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.
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.</description><subject>Bioinformatics</subject><subject>Breast cancer</subject><subject>breast neoplasms</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer</subject><subject>Cancer cells</subject><subject>Carcinogenesis</subject><subject>Chromatin</subject><subject>Chromatin - genetics</subject><subject>Chromosomes</subject><subject>Comparative analysis</subject><subject>Development and progression</subject><subject>Discovery tools</subject><subject>Epigenesis, Genetic</subject><subject>Epigenetic inheritance</subject><subject>epigenetics</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - metabolism</subject><subject>Epithelial Cells - pathology</subject><subject>epithelium</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic research</subject><subject>genome</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Humans</subject><subject>Mammary Glands, Human - metabolism</subject><subject>Mammary Glands, Human - pathology</subject><subject>MCF-7 Cells</subject><subject>Morphology</subject><subject>neoplasm cells</subject><subject>Patient outcomes</subject><subject>Stem cells</subject><subject>Telomere - genetics</subject><subject>Telomeres</subject><subject>Tumor cell lines</subject><subject>Tumorigenesis</subject><subject>Wnt protein</subject><issn>1474-760X</issn><issn>1474-7596</issn><issn>1474-760X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>KPI</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkkFvFCEYhidGY-vqD_BiJvFSD1NhhgHmYtJstDY20YMm3gjLfOzSMLACU-0P8H_7bbc2XS-GAwSe9_2A762ql5ScUir520w70g8NoX1DBJcNeVQdUyZYIzj5_vjB-qh6lvMVIXRgLX9aHbWc0V7K9rj6vdykOOniQu1CgaRNcTHUOmh_k12uE1yD9rk2Gx3WkBGq86S9xw3UxRwnQHisC3hcJqiNnzP6uLCuV1B-AoQatq5swDvtb9FVAp1LbXQwkGoD3ufn1ROLVeDF3byovn14_3X5sbn8fH6xPLtsDOe0NKyXPVsJQWUnJWXd2BLJhNGUDa1hpOOjgZWgIzF2tIYLau1gqTCjHaXVLe8W1bu973ZeTYB0KEl7tU1u0ulGRe3U4UlwG7WO1worCy4GNDi5M0jxxwy5qMnl3RN0gDhn1RJC2oHSjv8XpfgM7NoOXlSv_0Gv4pywBWjYEtHTnjGJ1OmeWmsPygUb8YoGxwiTMzGAdbh_1mNrh460DAVvDgTIFPhV1nrOWX36cnHI0j1rUsw5gb3_FErULmxqHzaFYVO7sCmCmlcPf_Ne8Tdd3R-b-dG4</recordid><startdate>20150928</startdate><enddate>20150928</enddate><creator>Barutcu, A Rasim</creator><creator>Lajoie, Bryan R</creator><creator>McCord, Rachel P</creator><creator>Tye, Coralee E</creator><creator>Hong, Deli</creator><creator>Messier, Terri L</creator><creator>Browne, Gillian</creator><creator>van Wijnen, Andre J</creator><creator>Lian, Jane B</creator><creator>Stein, Janet L</creator><creator>Dekker, Job</creator><creator>Imbalzano, Anthony N</creator><creator>Stein, Gary S</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>KPI</scope><scope>IAO</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope><scope>5PM</scope></search><sort><creationdate>20150928</creationdate><title>Chromatin interaction analysis reveals changes in small chromosome and telomere clustering between epithelial and breast cancer cells</title><author>Barutcu, A Rasim ; Lajoie, Bryan R ; McCord, Rachel P ; Tye, Coralee E ; Hong, Deli ; Messier, Terri L ; Browne, Gillian ; van Wijnen, Andre J ; Lian, Jane B ; Stein, Janet L ; Dekker, Job ; Imbalzano, Anthony N ; Stein, Gary S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c661t-45854b7718388143d20847ca1492c4036dceb71d0cfdfc671ff9f17cdfd8fa263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Bioinformatics</topic><topic>Breast cancer</topic><topic>breast neoplasms</topic><topic>Breast Neoplasms - 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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.
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.
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.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26415882</pmid><doi>10.1186/s13059-015-0768-0</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Bioinformatics Breast cancer breast neoplasms Breast Neoplasms - genetics Breast Neoplasms - pathology Cancer Cancer cells Carcinogenesis Chromatin Chromatin - genetics Chromosomes Comparative analysis Development and progression Discovery tools Epigenesis, Genetic Epigenetic inheritance epigenetics Epithelial cells Epithelial Cells - metabolism Epithelial Cells - pathology epithelium Female Gene expression Gene Expression Regulation, Neoplastic Genes Genetic aspects Genetic research genome Genomes Genomics Humans Mammary Glands, Human - metabolism Mammary Glands, Human - pathology MCF-7 Cells Morphology neoplasm cells Patient outcomes Stem cells Telomere - genetics Telomeres Tumor cell lines Tumorigenesis Wnt protein |
title | Chromatin interaction analysis reveals changes in small chromosome and telomere clustering between epithelial and breast cancer cells |
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