دورية أكاديمية
أعرض في EDS

ZMIZ1 enhances ERα-dependent expression of E2F2 in breast cancer.

التفاصيل البيبلوغرافية
العنوان: ZMIZ1 enhances ERα-dependent expression of E2F2 in breast cancer.
المؤلفون: Zhao W; Department of Biology, University of York, York, UK., Rose SF; Department of Biology, University of York, York, UK., Blake R; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK., Godicelj A; Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Smith Building, Boston, Massachusetts, USA., Cullen AE; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK., Stenning J; Department of Biology, University of York, York, UK., Beevors L; The Institute of Metabolism and Systems Research (IMSR), University of Birmingham, College of Medical and Dental Sciences, Birmingham, UK., Gehrung M; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK., Kumar S; Chris O'Brien Lifehouse, Sydney, New South Wales, Australia., Kishore K; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK., Sawle A; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK., Eldridge M; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK., Giorgi FM; Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy., Bridge KS; Department of Biology, University of York, York, UK.; York Biomedical Research Institute, University of York, York, UK., Markowetz F; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK., Holding AN; Department of Biology, University of York, York, UK.; York Biomedical Research Institute, University of York, York, UK.; The Alan Turing Institute, Kings Cross, London, UK.
المصدر: Journal of molecular endocrinology [J Mol Endocrinol] 2024 Apr 25; Vol. 73 (1). Date of Electronic Publication: 2024 Apr 25 (Print Publication: 2024).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: BioScientifica Country of Publication: England NLM ID: 8902617 Publication Model: Electronic-Print Cited Medium: Internet ISSN: 1479-6813 (Electronic) Linking ISSN: 09525041 NLM ISO Abbreviation: J Mol Endocrinol Subsets: MEDLINE
أسماء مطبوعة: Publication: Jan. 2011- : Bristol, UK : BioScientifica
Original Publication: Bristol, U.K. : Journal of Endocrinology, Ltd., c1988-
مواضيع طبية MeSH: Breast Neoplasms*/metabolism , Breast Neoplasms*/genetics , Breast Neoplasms*/pathology , Estrogen Receptor alpha*/metabolism , Estrogen Receptor alpha*/genetics , Gene Expression Regulation, Neoplastic* , E2F2 Transcription Factor*/metabolism , E2F2 Transcription Factor*/genetics, Humans ; Female ; Cell Line, Tumor ; Cell Proliferation/genetics ; Transcription Factors/metabolism ; Transcription Factors/genetics ; Protein Binding ; Promoter Regions, Genetic/genetics ; Signal Transduction ; Cell Cycle/genetics ; Prognosis
مستخلص: The estrogen receptor-α (ER) drives 75% of breast cancers. On activation, the ER recruits and assembles a 1-2 MDa transcriptionally active complex. These complexes can modulate tumour growth, and understanding the roles of individual proteins within these complexes can help identify new therapeutic targets. Here, we present the discovery of ER and ZMIZ1 within the same multi-protein assembly by quantitative proteomics, and validated by proximity ligation assay. We characterise ZMIZ1 function by demonstrating a significant decrease in the proliferation of ER-positive cancer cell lines. To establish a role for the ER-ZMIZ1 interaction, we measured the transcriptional changes in the estrogen response post-ZMIZ1 knockdown using an RNA-seq time-course over 24 h. Gene set enrichment analysis of the ZMIZ1-knockdown data identified a specific delay in the response of estradiol-induced cell cycle genes. Integration of ENCODE data with our RNA-seq results identified that ER and ZMIZ1 both bind the promoter of E2F2. We therefore propose that ER and ZMIZ1 interact to enable the efficient estrogenic response at subset of cell cycle genes via a novel ZMIZ1-ER-E2F2 signalling axis. Finally, we show that high ZMIZ1 expression is predictive of worse patient outcome, ER and ZMIZ1 are co-expressed in breast cancer patients in TCGA and METABRIC, and the proteins are co-localised within the nuclei of tumour cell in patient biopsies. In conclusion, we establish that ZMIZ1 is a regulator of the estrogenic cell cycle response and provide evidence of the biological importance of the ER-ZMIZ1 interaction in ER-positive patient tumours, supporting potential clinical relevance.
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فهرسة مساهمة: Keywords: E2F2; ZMIZ1; breast cancer; cancer; co-factors transcription nuclear receptors signalling patient outcome; estrogen receptor
المشرفين على المادة: 0 (Estrogen Receptor alpha)
0 (E2F2 Transcription Factor)
0 (Transcription Factors)
0 (E2F2 protein, human)
0 (ESR1 protein, human)
تواريخ الأحداث: Date Created: 20240402 Date Completed: 20240425 Latest Revision: 20240522
رمز التحديث: 20240522
مُعرف محوري في PubMed: PMC11103680
DOI: 10.1530/JME-23-0133
PMID: 38564418
قاعدة البيانات: MEDLINE
الوصف
تدمد:1479-6813
DOI:10.1530/JME-23-0133