A bi-stable feedback loop between GDNF, EGR1, and ERα contribute to endocrine resistant breast cancer
Publication Date
April 03, 2018
Authors
Sachi Horibata, Edward J. Rice, Hui Zheng, Chinatsu Mukai, et al
Volume
13
Issue
4
Pages
e0194522
DOI
http://doi.org/10.1371/journal.pone.0194522
Publisher URL
http://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0194522
Scopus
85044988841
Mendeley
http://www.mendeley.com/research/bistable-feedback-loop-between-gdnf-egr1-er%CE%B1-contribute-endocrine-resistant-breast-cancer
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Mendeley | Further Information

{"title"=>"A bi-stable feedback loop between GDNF, EGR1, and ERα contribute to endocrine resistant breast cancer", "type"=>"journal", "authors"=>[{"first_name"=>"Sachi", "last_name"=>"Horibata", "scopus_author_id"=>"35487508700"}, {"first_name"=>"Edward J.", "last_name"=>"Rice", "scopus_author_id"=>"57200860814"}, {"first_name"=>"Hui", "last_name"=>"Zheng", "scopus_author_id"=>"57201450315"}, {"first_name"=>"Chinatsu", "last_name"=>"Mukai", "scopus_author_id"=>"57201450596"}, {"first_name"=>"Tinyi", "last_name"=>"Chu", "scopus_author_id"=>"57195369392"}, {"first_name"=>"Brooke A.", "last_name"=>"Marks", "scopus_author_id"=>"57199326261"}, {"first_name"=>"Scott A.", "last_name"=>"Coonrod", "scopus_author_id"=>"35587818200"}, {"first_name"=>"Charles G.", "last_name"=>"Danko", "scopus_author_id"=>"23484848900"}], "year"=>2018, "source"=>"PLoS ONE", "identifiers"=>{"scopus"=>"2-s2.0-85044988841", "pui"=>"621516735", "issn"=>"19326203", "doi"=>"10.1371/journal.pone.0194522", "sgr"=>"85044988841"}, "id"=>"362611e7-8c12-3f25-a440-502edadfcd13", "abstract"=>"Discovering regulatory interactions between genes that specify the behavioral properties of cells remains an important challenge. We used the dynamics of transcriptional changes resolved by PRO-seq to identify a regulatory network responsible for endocrine resistance in breast cancer. We show that GDNF leads to endocrine resistance by switching the active state in a bi-stable feedback loop between GDNF, EGR1, and the master transcription factor ERα. GDNF stimulates MAP kinase, activating the transcription factors SRF and AP-1. SRF initiates an immediate transcriptional response, activating EGR1 and suppressing ERα. Newly translated EGR1 protein activates endogenous GDNF, leading to constitutive GDNF and EGR1 up-regulation, and the sustained down-regulation of ERα. Endocrine resistant MCF-7 cells are constitutively in the GDNF-high/ ERα-low state, suggesting that the state in the bi-stable feedback loop may provide a ‘memory’ of endocrine resistance. Thus, we identified a regulatory network switch that contributes to drug resistance in breast cancer.", "link"=>"http://www.mendeley.com/research/bistable-feedback-loop-between-gdnf-egr1-er%CE%B1-contribute-endocrine-resistant-breast-cancer", "reader_count"=>2, "reader_count_by_academic_status"=>{"Researcher"=>1, "Student > Master"=>1}, "reader_count_by_user_role"=>{"Researcher"=>1, "Student > Master"=>1}, "reader_count_by_subject_area"=>{"Chemical Engineering"=>1, "Pharmacology, Toxicology and Pharmaceutical Science"=>1}, "reader_count_by_subdiscipline"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}, "Chemical Engineering"=>{"Chemical Engineering"=>1}}, "group_count"=>1}

Scopus | Further Information

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