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Tytuł:
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Overexpression and alternative splicing of NF-YA in breast cancer.
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Autorzy:
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Dolfini D; Dipartimento di Bioscienze, Università degli Studi di Milano, Via Celoria 26, 20133, Milano, Italy.
Andrioletti V; Dipartimento di Bioscienze, Università degli Studi di Milano, Via Celoria 26, 20133, Milano, Italy.; Internal Medicine VIII, University Hospital Tübingen, Otfried-Müller-Str. 14, 72076, Tübingen, Germany.
Mantovani R; Dipartimento di Bioscienze, Università degli Studi di Milano, Via Celoria 26, 20133, Milano, Italy. .
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Źródło:
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Scientific reports [Sci Rep] 2019 Sep 10; Vol. 9 (1), pp. 12955. Date of Electronic Publication: 2019 Sep 10.
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Typ publikacji:
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Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Original Publication: London : Nature Publishing Group, copyright 2011-
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MeSH Terms:
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Alternative Splicing*
BRCA1 Protein/*metabolism
BRCA2 Protein/*metabolism
Biomarkers, Tumor/*genetics
Breast Neoplasms/*pathology
CCAAT-Binding Factor/*genetics
E2F Transcription Factors/*metabolism
BRCA1 Protein/genetics ; BRCA2 Protein/genetics ; Biomarkers, Tumor/metabolism ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; CCAAT-Binding Factor/metabolism ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; E2F Transcription Factors/genetics ; Female ; Gene Expression Profiling ; Humans ; Promoter Regions, Genetic ; Protein Binding ; Tumor Cells, Cultured
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References:
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PLoS Comput Biol. 2017 Jan 19;13(1):e1005340. (PMID: 28103241)
Stem Cells Int. 2017;2017:5091541. (PMID: 28392805)
Biochim Biophys Acta Gene Regul Mech. 2017 May;1860(5):604-616. (PMID: 27939755)
J Biol Chem. 2009 Dec 4;284(49):34189-200. (PMID: 19690168)
J Biol Chem. 2002 Feb 15;277(7):5168-74. (PMID: 11744689)
Bioinformatics. 2016 Apr 1;32(7):1097-9. (PMID: 26607490)
Oncotarget. 2016 Jan 12;7(2):1633-50. (PMID: 26646448)
BMC Med Genomics. 2015 Aug 22;8:54. (PMID: 26297356)
Cancer Inform. 2013;12:31-51. (PMID: 23470717)
Nucleic Acids Res. 2011 May;39(9):3558-73. (PMID: 21247883)
Biomark Cancer. 2010 Feb 11;2:1-15. (PMID: 24179381)
Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W199-203. (PMID: 15215380)
Genome Biol. 2013;14(10):R110. (PMID: 24176112)
Cell. 2015 Oct 8;163(2):506-19. (PMID: 26451490)
BMC Syst Biol. 2010 May 27;4:74. (PMID: 20507583)
Cancer Res. 2016 Feb 1;76(3):664-74. (PMID: 26589882)
Genes Cancer. 2011 Oct;2(10):979-84. (PMID: 22701763)
Proc Natl Acad Sci U S A. 2014 Aug 26;111(34):12550-5. (PMID: 25114226)
Nucleic Acids Res. 2016 Jun 2;44(10):4684-702. (PMID: 26896797)
Mol Biol Cell. 2008 Dec;19(12):5203-13. (PMID: 18815279)
Blood. 2010 Oct 14;116(15):2676-83. (PMID: 20616221)
Mol Biol Cell. 2003 Jul;14(7):2706-15. (PMID: 12857858)
Stem Cells. 2012 Nov;30(11):2450-9. (PMID: 22969033)
BMC Genomics. 2014 Nov 21;15:1008. (PMID: 25412710)
Biochim Biophys Acta Gene Regul Mech. 2017 May;1860(5):590-597. (PMID: 27697431)
J Cancer. 2017 Sep 12;8(16):3131-3141. (PMID: 29158785)
Nature. 2012 Oct 4;490(7418):61-70. (PMID: 23000897)
Cell. 2016 Jun 2;165(6):1375-1388. (PMID: 27259149)
Nature. 2000 Aug 17;406(6797):747-52. (PMID: 10963602)
Breast Cancer Res. 2010;12(5):R68. (PMID: 20813035)
Cell Death Differ. 2013 May;20(5):676-85. (PMID: 23449390)
Biochim Biophys Acta Gene Regul Mech. 2017 May;1860(5):571-580. (PMID: 27677949)
Onco Targets Ther. 2016 May 02;9:2593-600. (PMID: 27217777)
Mol Cell. 2009 Dec 11;36(5):900-11. (PMID: 20005852)
J Biol Chem. 1992 May 5;267(13):8984-90. (PMID: 1577736)
Genome Res. 2013 Aug;23(8):1195-209. (PMID: 23595228)
Oncol Lett. 2018 Jun;15(6):9216-9230. (PMID: 29844824)
Oncotarget. 2017 Jan 31;8(5):7935-7945. (PMID: 27974701)
Breast Cancer Res Treat. 2013 Nov;142(2):237-55. (PMID: 24162158)
Biochim Biophys Acta Gene Regul Mech. 2017 May;1860(5):581-589. (PMID: 27769808)
Nucleic Acids Res. 2009 Jul;37(Web Server issue):W247-52. (PMID: 19487240)
Exp Dermatol. 2014 Oct;23 Suppl 1:2-6. (PMID: 25234828)
Cancer Cell. 2015 May 11;27(5):712-27. (PMID: 25965574)
BMC Med Genomics. 2012 Oct 04;5:44. (PMID: 23035882)
Int J Oncol. 2018 Nov;53(5):1857-1868. (PMID: 30106137)
Acta Histochem. 2012 Oct;114(6):553-61. (PMID: 22104449)
Neurosci Lett. 2016 Sep 19;631:40-49. (PMID: 27495011)
Nat Commun. 2014 Nov 19;5:5323. (PMID: 25406515)
Blood. 1999 Jan 15;93(2):519-26. (PMID: 9885213)
Mol Cell. 2014 Sep 4;55(5):708-22. (PMID: 25132174)
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Substance Nomenclature:
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0 (BRCA1 Protein)
0 (BRCA1 protein, human)
0 (BRCA2 Protein)
0 (BRCA2 protein, human)
0 (Biomarkers, Tumor)
0 (CCAAT-Binding Factor)
0 (E2F Transcription Factors)
0 (NFYA protein, human)
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Entry Date(s):
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Date Created: 20190912 Date Completed: 20201030 Latest Revision: 20210110
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Update Code:
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20240105
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PubMed Central ID:
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PMC6736888
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DOI:
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10.1038/s41598-019-49297-5
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PMID:
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31506469
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NF-Y is a CCAAT-binding trimeric transcription factor, whose regulome, interactome and oncogenic potential point to direct involvement in cellular transformation. Yet little is known about the levels of NF-Y subunits in tumors. We focused on breast carcinomas, and analyzed RNA-Seq datasets of TCGA and 54 BRCA cell lines at gene and isoforms level. We partitioned all tumors in the four major subclasses. NF-YA, but not histone-fold subunits NF-YB/NF-YC, is globally overexpressed, correlating with the proliferative Ki67 marker and a common set of 840 genes, with cell-cycle, metabolism GO terms. Their promoters are enriched in NF-Y, GC-rich and E2F sites. Surprisingly, there is an isoform switch, with the "short" isoform -NF-YAs- becoming predominant in tumors. E2F genes are also overexpressed in BRCA, but no switch in isoforms is observed. In Basal-like Claudin low cell lines and tumors, expression of NF-YAl -long- isoform is high, together with 11 typical EMT markers and low levels of basal Keratins. Analysis of Progression-Free-Intervals indicates that tumors with unbalance of NF-YA isoforms ratios have worst clinical outcomes. The data suggest that NF-YA overexpression increases CCAAT-dependent, pro-growth genes in BRCA. NF-YAs is associated with a proliferative signature, but high levels of NF-YAl signal loss of epithelial features, EMT and acquisition of a more aggressive behavior in a subset of Claudin low Basal-like tumors.
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