{"doi":"10.1073/pnas.1612835113","title":"FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer","abstract":"<jats:title>Significance</jats:title>\n                  <jats:p>\n                    One of the mechanisms of endocrine resistance in estrogen receptor α (ER)-positive (\n                    <jats:sup>+</jats:sup>\n                    ) breast cancer is the cross-talk between the ER and growth factor receptor pathways leading to altered ER activity and a reprogrammed ER-dependent transcriptome. However, key mediators of this ER-dependent transcriptional reprogramming remain elusive. Here we demonstrate that forkhead box protein A1 (FOXA1) up-regulation via gene amplification or overexpression contributes to endocrine resistance and increased invasiveness phenotypes by altering the ER-dependent transcriptome. We further show that IL-8, one of the top altered FOXA1/ER effectors, plays a key role in mediating these phenotypes and is a potential target to treat ER\n                    <jats:sup>+</jats:sup>\n                    /FOXA1-high breast cancer. Our findings provoke a new interplay of FOXA1 in the ER transcriptional program in endocrine-resistant breast cancer.\n                  </jats:p>","journal":"Proceedings of the National Academy of Sciences","year":2016,"id":602854,"datarank":0.7838620010569803,"base_score":5.225746673713202,"endowment":5.225746673713202,"self_citation_contribution":0.7838620010569803,"citation_network_contribution":0.0,"self_endowment_contribution":0.7838620010569803,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":185,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":565777,"name":"Rinath Jeselsohn","orcid":"0000-0001-7996-7529","position":1,"is_corresponding":false},{"id":639739,"name":"Resel Pereira","orcid":null,"position":2,"is_corresponding":false},{"id":1546299,"name":"Emporia F. 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Grasso","orcid":"0000-0001-8632-4126","position":12,"is_corresponding":false},{"id":1842,"name":"Paul T. Spellman","orcid":"0000-0002-4810-0022","position":13,"is_corresponding":false},{"id":231288,"name":"Obi L. Griffith","orcid":"0000-0002-0843-4271","position":14,"is_corresponding":false},{"id":44714,"name":"Anna Tsimelzon","orcid":null,"position":15,"is_corresponding":false},{"id":1546317,"name":"Carolina Gutierrez","orcid":null,"position":16,"is_corresponding":false},{"id":2210,"name":"Shixia Huang","orcid":"0000-0003-2878-4129","position":17,"is_corresponding":false},{"id":2211,"name":"Dean P. Edwards","orcid":null,"position":18,"is_corresponding":false},{"id":708904,"name":"Meghana V. Trivedi","orcid":"0000-0002-0585-5580","position":19,"is_corresponding":false},{"id":270275,"name":"Mothaffar F. 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Kent Osborne","orcid":"0000-0002-0044-618X","position":25,"is_corresponding":false},{"id":263252,"name":"Rachel Schiff","orcid":"0000-0003-1696-5213","position":26,"is_corresponding":false},{"id":263244,"name":"Xiaoyong Fu","orcid":"0000-0003-0005-6496","position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"FOXA1 overexpression mediates endocrine resistance by altering the ER transcriptome and IL-8 expression in ER-positive breast cancer","abstract":"<jats:title>Significance</jats:title>\n                  <jats:p>\n                    One of the mechanisms of endocrine resistance in estrogen receptor α (ER)-positive (\n                    <jats:sup>+</jats:sup>\n                    ) breast cancer is the cross-talk between the ER and growth factor receptor pathways leading to altered ER activity and a reprogrammed ER-dependent transcriptome. However, key mediators of this ER-dependent transcriptional reprogramming remain elusive. Here we demonstrate that forkhead box protein A1 (FOXA1) up-regulation via gene amplification or overexpression contributes to endocrine resistance and increased invasiveness phenotypes by altering the ER-dependent transcriptome. We further show that IL-8, one of the top altered FOXA1/ER effectors, plays a key role in mediating these phenotypes and is a potential target to treat ER\n                    <jats:sup>+</jats:sup>\n                    /FOXA1-high breast cancer. Our findings provoke a new interplay of FOXA1 in the ER transcriptional program in endocrine-resistant breast cancer.\n                  </jats:p>","is_dataset_classified":null,"base_score":5.225746673713202,"endowment":5.225746673713202,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"27791031","pmcid":"PMC5087040","openalex_id":"https://openalex.org/W2529485187","authors":[],"funders":[{"funder_name":"DOD | Congressionally Directed Medical Research Programs","grant_id":"W81XWH-14-1-0326","title":null},{"funder_name":"Breast Cancer Research Foundation","grant_id":"BCRF","title":null},{"funder_name":"American Association for Cancer Research","grant_id":"SU2C-AACR-DT0409","title":null},{"funder_name":"HHS | NIH | National Cancer Institute","grant_id":"Breast Cancer SPORE","title":null},{"funder_name":"HHS | NIH | National Cancer Institute","grant_id":"P30CA125123","title":null},{"funder_name":"Susan G. 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