An integrative epigenomic approach identifies ELF3 as an oncogenic regulator in ASCL1‐positive neuroendocrine carcinoma
Neuroendocrine carcinoma (NEC) is a highly aggressive subtype of the neuroendocrine tumor with an extremely poor prognosis. We have previously conducted a comprehensive genomic analysis of over 100 cases of NEC of the gastrointestinal system (GIS‐NEC) and unraveled its unique and organ‐specific geno...
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| Veröffentlicht in: | Cancer science 2023-06, Vol.114 (6), p.2596-2608 |
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| creator | Horie, Masafumi Tanaka, Hidenori Suzuki, Masami Sato, Yoshihiko Takata, So Takai, Erina Miyashita, Naoya Saito, Akira Nakatani, Yoichiro Yachida, Shinichi |
| description | Neuroendocrine carcinoma (NEC) is a highly aggressive subtype of the neuroendocrine tumor with an extremely poor prognosis. We have previously conducted a comprehensive genomic analysis of over 100 cases of NEC of the gastrointestinal system (GIS‐NEC) and unraveled its unique and organ‐specific genomic drivers. However, the epigenomic features of GIS‐NEC remain unexplored. In this study, we have described the epigenomic landscape of GIS‐NEC and small cell lung carcinoma (SCLC) by integrating motif enrichment analysis from the assay of transposase‐accessible chromatin sequencing (ATAC‐seq) and enhancer profiling from a novel cleavage under targets and tagmentation (CUT&Tag) assay for H3K27ac and identified ELF3 as one of the super‐enhancer–related transcriptional factors in NEC. By combining CUT&Tag and knockdown RNA sequencing for ELF3, we uncovered the transcriptional network regulated by ELF3 and defined its distinctive gene signature, including AURKA, CDC25B, CLDN4, ITGB6, and YWAHB. Furthermore, a loss‐of‐function assay revealed that ELF3 depletion led to poor cell viability. Finally, using gene expression of clinical samples, we successfully divided GIS‐NEC patients into two subgroups according to the ELF3 signature and demonstrated that tumor‐promoting pathways were activated in the ELF3 signature–high group. Our findings highlight the transcriptional regulation of ELF3 as an oncogenic transcription factor and its tumor‐promoting properties in NEC.
Multiorgan comprehensive epigenomic analysis identified ELF3 as a super‐enhancer–associated transcription factor and revealed its oncogenic properties in neuroendocrine carcinoma. |
| doi_str_mv | 10.1111/cas.15764 |
| format | Article |
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Multiorgan comprehensive epigenomic analysis identified ELF3 as a super‐enhancer–associated transcription factor and revealed its oncogenic properties in neuroendocrine carcinoma.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.15764</identifier><identifier>PMID: 36840413</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Antibodies ; ASCL1 protein ; ATAC‐seq ; Cancer ; Cdc25B phosphatase ; Cell cycle ; Cell viability ; Chromatin ; Cloning ; CUT&Tag ; ELF3 ; Gene expression ; Gene regulation ; Genomes ; Genomic analysis ; Lung carcinoma ; neuroendocrine carcinoma ; Neuroendocrine tumors ; Original ; ORIGINAL ARTICLES ; Signal transduction ; Small cell lung carcinoma ; Statistical significance ; super‐enhancer ; Transcription factors ; Transposase</subject><ispartof>Cancer science, 2023-06, Vol.114 (6), p.2596-2608</ispartof><rights>2023 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2023 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2023. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5344-f0548b8ae8133dc6c819a19aa721efaaec2693f360b8385b8d86cba663d96e063</citedby><cites>FETCH-LOGICAL-c5344-f0548b8ae8133dc6c819a19aa721efaaec2693f360b8385b8d86cba663d96e063</cites><orcidid>0000-0002-7726-4077 ; 0000-0001-5507-4566 ; 0000-0002-2464-5167 ; 0000-0002-0184-1376 ; 0000-0002-8071-1077</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10236617/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10236617/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36840413$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Horie, Masafumi</creatorcontrib><creatorcontrib>Tanaka, Hidenori</creatorcontrib><creatorcontrib>Suzuki, Masami</creatorcontrib><creatorcontrib>Sato, Yoshihiko</creatorcontrib><creatorcontrib>Takata, So</creatorcontrib><creatorcontrib>Takai, Erina</creatorcontrib><creatorcontrib>Miyashita, Naoya</creatorcontrib><creatorcontrib>Saito, Akira</creatorcontrib><creatorcontrib>Nakatani, Yoichiro</creatorcontrib><creatorcontrib>Yachida, Shinichi</creatorcontrib><title>An integrative epigenomic approach identifies ELF3 as an oncogenic regulator in ASCL1‐positive neuroendocrine carcinoma</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Neuroendocrine carcinoma (NEC) is a highly aggressive subtype of the neuroendocrine tumor with an extremely poor prognosis. We have previously conducted a comprehensive genomic analysis of over 100 cases of NEC of the gastrointestinal system (GIS‐NEC) and unraveled its unique and organ‐specific genomic drivers. However, the epigenomic features of GIS‐NEC remain unexplored. In this study, we have described the epigenomic landscape of GIS‐NEC and small cell lung carcinoma (SCLC) by integrating motif enrichment analysis from the assay of transposase‐accessible chromatin sequencing (ATAC‐seq) and enhancer profiling from a novel cleavage under targets and tagmentation (CUT&Tag) assay for H3K27ac and identified ELF3 as one of the super‐enhancer–related transcriptional factors in NEC. By combining CUT&Tag and knockdown RNA sequencing for ELF3, we uncovered the transcriptional network regulated by ELF3 and defined its distinctive gene signature, including AURKA, CDC25B, CLDN4, ITGB6, and YWAHB. Furthermore, a loss‐of‐function assay revealed that ELF3 depletion led to poor cell viability. Finally, using gene expression of clinical samples, we successfully divided GIS‐NEC patients into two subgroups according to the ELF3 signature and demonstrated that tumor‐promoting pathways were activated in the ELF3 signature–high group. Our findings highlight the transcriptional regulation of ELF3 as an oncogenic transcription factor and its tumor‐promoting properties in NEC.
Multiorgan comprehensive epigenomic analysis identified ELF3 as a super‐enhancer–associated transcription factor and revealed its oncogenic properties in neuroendocrine carcinoma.</description><subject>Antibodies</subject><subject>ASCL1 protein</subject><subject>ATAC‐seq</subject><subject>Cancer</subject><subject>Cdc25B phosphatase</subject><subject>Cell cycle</subject><subject>Cell viability</subject><subject>Chromatin</subject><subject>Cloning</subject><subject>CUT&Tag</subject><subject>ELF3</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Genomes</subject><subject>Genomic analysis</subject><subject>Lung carcinoma</subject><subject>neuroendocrine carcinoma</subject><subject>Neuroendocrine tumors</subject><subject>Original</subject><subject>ORIGINAL ARTICLES</subject><subject>Signal transduction</subject><subject>Small cell lung carcinoma</subject><subject>Statistical significance</subject><subject>super‐enhancer</subject><subject>Transcription factors</subject><subject>Transposase</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kctq3DAUhkVpaS7toi9QBN20CyeSJcvyqgxDbjDQRdq1OJaPJwoeyZXshNn1EfqMfZIqM0loCxUCCfTxnXP0E_KOsxOe16mFdMKrWskX5JAL2RQ1Y-rl7l4XDRPlATlK6ZYxoWQjX5MDobRkkotDsl146vyE6wiTu0OKo1ujDxtnKYxjDGBvqOvQT653mOjZ6lxQSBQ8Dd6GjGYw4noeYAoxm-jierniv378HENyO6PHOQb0XbDReaQWonW5ALwhr3oYEr59PI_Jt_Ozr8vLYvXl4mq5WBW2ElIWPaukbjWg5kJ0VlnNG8gb6pJjD4C2VI3ohWKtFrpqdaeVbUEp0TUKmRLH5PPeO87tBjubZ4kwmDG6DcStCeDM3y_e3Zh1uDOclUIpXmfDx0dDDN9nTJPZuGRxGMBjmJMpa53_W3EtM_rhH_Q2zNHn-Uypy5xRVdciU5_2lI0hpYj9czecmYdETU7U7BLN7Ps_238mnyLMwOkeuHcDbv9vMsvF9V75G7FqrTo</recordid><startdate>202306</startdate><enddate>202306</enddate><creator>Horie, Masafumi</creator><creator>Tanaka, Hidenori</creator><creator>Suzuki, Masami</creator><creator>Sato, Yoshihiko</creator><creator>Takata, So</creator><creator>Takai, Erina</creator><creator>Miyashita, Naoya</creator><creator>Saito, Akira</creator><creator>Nakatani, Yoichiro</creator><creator>Yachida, Shinichi</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</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>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PKEHL</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7726-4077</orcidid><orcidid>https://orcid.org/0000-0001-5507-4566</orcidid><orcidid>https://orcid.org/0000-0002-2464-5167</orcidid><orcidid>https://orcid.org/0000-0002-0184-1376</orcidid><orcidid>https://orcid.org/0000-0002-8071-1077</orcidid></search><sort><creationdate>202306</creationdate><title>An integrative epigenomic approach identifies ELF3 as an oncogenic regulator in ASCL1‐positive neuroendocrine carcinoma</title><author>Horie, Masafumi ; 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We have previously conducted a comprehensive genomic analysis of over 100 cases of NEC of the gastrointestinal system (GIS‐NEC) and unraveled its unique and organ‐specific genomic drivers. However, the epigenomic features of GIS‐NEC remain unexplored. In this study, we have described the epigenomic landscape of GIS‐NEC and small cell lung carcinoma (SCLC) by integrating motif enrichment analysis from the assay of transposase‐accessible chromatin sequencing (ATAC‐seq) and enhancer profiling from a novel cleavage under targets and tagmentation (CUT&Tag) assay for H3K27ac and identified ELF3 as one of the super‐enhancer–related transcriptional factors in NEC. By combining CUT&Tag and knockdown RNA sequencing for ELF3, we uncovered the transcriptional network regulated by ELF3 and defined its distinctive gene signature, including AURKA, CDC25B, CLDN4, ITGB6, and YWAHB. Furthermore, a loss‐of‐function assay revealed that ELF3 depletion led to poor cell viability. Finally, using gene expression of clinical samples, we successfully divided GIS‐NEC patients into two subgroups according to the ELF3 signature and demonstrated that tumor‐promoting pathways were activated in the ELF3 signature–high group. Our findings highlight the transcriptional regulation of ELF3 as an oncogenic transcription factor and its tumor‐promoting properties in NEC.
Multiorgan comprehensive epigenomic analysis identified ELF3 as a super‐enhancer–associated transcription factor and revealed its oncogenic properties in neuroendocrine carcinoma.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>36840413</pmid><doi>10.1111/cas.15764</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-7726-4077</orcidid><orcidid>https://orcid.org/0000-0001-5507-4566</orcidid><orcidid>https://orcid.org/0000-0002-2464-5167</orcidid><orcidid>https://orcid.org/0000-0002-0184-1376</orcidid><orcidid>https://orcid.org/0000-0002-8071-1077</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antibodies ASCL1 protein ATAC‐seq Cancer Cdc25B phosphatase Cell cycle Cell viability Chromatin Cloning CUT&Tag ELF3 Gene expression Gene regulation Genomes Genomic analysis Lung carcinoma neuroendocrine carcinoma Neuroendocrine tumors Original ORIGINAL ARTICLES Signal transduction Small cell lung carcinoma Statistical significance super‐enhancer Transcription factors Transposase |
| title | An integrative epigenomic approach identifies ELF3 as an oncogenic regulator in ASCL1‐positive neuroendocrine carcinoma |
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