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Tytuł pozycji:

ETV4 plays a role on the primary events during the adenoma-adenocarcinoma progression in colorectal cancer.

Tytuł :
ETV4 plays a role on the primary events during the adenoma-adenocarcinoma progression in colorectal cancer.
Autorzy :
Fonseca AS; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Av Bandeirantes, 3900, CEP: 14049-900, Monte Alegre, Ribeirão Preto, SP, Brazil. .; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil. .; Center for Integrative Systems Biology - CISBi, NAP/USP, Ribeirão Preto, SP, Brazil. .; Research Institute Pelé Pequeno Príncipe, Av Silva Jardim, 1632, CEP: 80250-060, Água Verde, Curitiba, PR, Brazil. .
Ramão A; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Av Bandeirantes, 3900, CEP: 14049-900, Monte Alegre, Ribeirão Preto, SP, Brazil.; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Bürger MC; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
de Souza JES; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Zanette DL; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Av Bandeirantes, 3900, CEP: 14049-900, Monte Alegre, Ribeirão Preto, SP, Brazil.; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.; Center for Integrative Systems Biology - CISBi, NAP/USP, Ribeirão Preto, SP, Brazil.; Laboratory of Applied Science and Technology in Health (LASTH), Instituto Carlos Chagas, Fundação Oswaldo Cruz, Curitiba, PR, Brazil.
de Molfetta GA; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Av Bandeirantes, 3900, CEP: 14049-900, Monte Alegre, Ribeirão Preto, SP, Brazil.; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.; Center for Integrative Systems Biology - CISBi, NAP/USP, Ribeirão Preto, SP, Brazil.
de Araújo LF; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Av Bandeirantes, 3900, CEP: 14049-900, Monte Alegre, Ribeirão Preto, SP, Brazil.; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.; Center for Integrative Systems Biology - CISBi, NAP/USP, Ribeirão Preto, SP, Brazil.
de Barros E Lima Bueno R; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Av Bandeirantes, 3900, CEP: 14049-900, Monte Alegre, Ribeirão Preto, SP, Brazil.; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Aguiar GM; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Plaça JR; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Alves CP; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Dos Santos ARD; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Vidal DO; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Silva GEB; Laboratory of Immunofluorescence and Electron Microscopy (LIME), Presidente Dutra University Hospital (HUUFMA), São Luís, MA, Brazil.
Panepucci RA; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Peria FM; Departament of Medical Clinic, Medical School of Ribeirão Preto, University of São Paulo, USP, Ribeirão Preto, SP, Brazil.
Feres O; Department of Surgery and Anatomy, School of Medicine of Ribeirão Preto, University of São Paulo, Sao Paulo, Brazil.
da Rocha JJR; Department of Surgery and Anatomy, School of Medicine of Ribeirão Preto, University of São Paulo, Sao Paulo, Brazil.
Zago MA; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil.
Silva WA Jr; Department of Genetics, Ribeirão Preto Medical School, University of São Paulo, Av Bandeirantes, 3900, CEP: 14049-900, Monte Alegre, Ribeirão Preto, SP, Brazil. .; Center for Cell Based Therapy and National Institute of Science and Technology in Stem Cell and Cell Therapy, Ribeirão Preto, SP, Brazil. .; Center for Integrative Systems Biology - CISBi, NAP/USP, Ribeirão Preto, SP, Brazil. .
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Źródło :
BMC cancer [BMC Cancer] 2021 Mar 01; Vol. 21 (1), pp. 207. Date of Electronic Publication: 2021 Mar 01.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Original Publication: London : BioMed Central, [2001-
MeSH Terms :
Genes, Neoplasm*
Adenocarcinoma/*genetics
Adenoma/*genetics
Colorectal Neoplasms/*genetics
Neoplasm Proteins/*physiology
Proto-Oncogene Proteins c-ets/*physiology
Adenocarcinoma/chemistry ; Adenocarcinoma/pathology ; Adenoma/chemistry ; Adenoma/pathology ; Aged ; Biomarkers, Tumor/genetics ; Brazil ; Cell Division/genetics ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Transformation, Neoplastic/genetics ; Colorectal Neoplasms/chemistry ; Colorectal Neoplasms/pathology ; DNA, Neoplasm/genetics ; Disease Progression ; Female ; Gene Expression Regulation, Neoplastic ; Gene Ontology ; Humans ; Male ; Middle Aged ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/genetics ; Proto-Oncogene Proteins c-ets/antagonists & inhibitors ; Proto-Oncogene Proteins c-ets/genetics ; RNA Interference ; RNA, Small Interfering/genetics ; RNA, Small Interfering/pharmacology ; Tissue Array Analysis ; Transcriptome ; Tumor Stem Cell Assay
References :
BMC Cancer. 2019 Jul 23;19(1):727. (PMID: 31337362)
Cell Tissue Res. 2014 Feb;355(2):365-74. (PMID: 24310606)
Cancer Biomark. 2019;24(4):485-495. (PMID: 30932884)
Bioinformatics. 2009 Feb 1;25(3):415-6. (PMID: 19106121)
Proc Natl Acad Sci U S A. 2013 Sep 10;110(37):E3506-15. (PMID: 23918374)
Nat Methods. 2014 Apr;11(4):361-2. (PMID: 24681721)
Biomed Res Int. 2018 Aug 6;2018:9416515. (PMID: 30175151)
Oncotarget. 2017 May 16;8(20):32783-32793. (PMID: 28427180)
Bioinformatics. 2003 Jan 22;19(2):185-93. (PMID: 12538238)
Cancer Biomark. 2017;19(1):57-64. (PMID: 28269751)
J Transl Med. 2015 Oct 27;13:337. (PMID: 26507719)
PLoS One. 2013 Apr 12;8(4):e60861. (PMID: 23593331)
Cancer Biomark. 2016 Mar 11;16(4):599-607. (PMID: 27002762)
Gut. 2007 Nov;56(11):1585-9. (PMID: 17591622)
Case Rep Pathol. 2012;2012:284064. (PMID: 23213588)
J Cell Biochem. 2018 Sep 1;:. (PMID: 30171715)
Bioorg Chem. 2020 Jan;95:103457. (PMID: 31901757)
Ann Surg. 1979 Dec;190(6):679-83. (PMID: 518167)
Oncol Lett. 2018 May;15(5):7000-7006. (PMID: 29731870)
Pathol Oncol Res. 2019 Oct;25(4):1589-1597. (PMID: 30710321)
J Clin Pathol. 2009 Dec;62(12):1096-102. (PMID: 19640859)
Pol J Pathol. 2010;61(1):8-22. (PMID: 20496268)
Gene. 2018 Dec 30;679:150-159. (PMID: 30193961)
Proc Natl Acad Sci U S A. 1992 May 15;89(10):4452-6. (PMID: 1316610)
Carcinogenesis. 2004 Mar;25(3):325-32. (PMID: 14604892)
Tumour Biol. 2015 May;36(5):3565-72. (PMID: 25544710)
BMC Gastroenterol. 2012 Mar 08;12:21. (PMID: 22400807)
Adv Exp Med Biol. 2000;480:107-16. (PMID: 10959416)
Clin Cancer Res. 2000 Mar;6(3):1086-92. (PMID: 10741738)
Br J Cancer. 2011 Jun 28;105(1):124-30. (PMID: 21673681)
Nucleic Acids Res. 1993 Feb 11;21(3):547-53. (PMID: 8441666)
Genome Biol. 2004;5(10):R80. (PMID: 15461798)
Bioinformatics. 2010 Jan 1;26(1):139-40. (PMID: 19910308)
BMC Cancer. 2018 Apr 16;18(1):433. (PMID: 29661177)
J Pathol. 2001 Mar;193(3):286-94. (PMID: 11241406)
Dis Markers. 2014;2014:634123. (PMID: 24959000)
Cell Adh Migr. 2019 Dec;13(1):273-284. (PMID: 31293204)
Genes Dev. 2011 Oct 15;25(20):2147-57. (PMID: 22012618)
Cell Biochem Biophys. 2015 Sep;73(1):253-9. (PMID: 25726157)
Cancer. 1975 Dec;36(6):2251-70. (PMID: 1203876)
Clin Transl Gastroenterol. 2019 Jun;10(6):e00053. (PMID: 31211760)
Hum Mutat. 2008 May;29(5):757-64. (PMID: 18348286)
Oncol Rep. 2006 Oct;16(4):747-54. (PMID: 16969489)
Nucleic Acids Res. 2016 May 5;44(8):e71. (PMID: 26704973)
Mol Carcinog. 2020 Jan;59(1):73-86. (PMID: 31670855)
Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
J Pathol. 2003 Aug;200(5):568-76. (PMID: 12898592)
Breast Cancer Res. 2018 Jul 11;20(1):73. (PMID: 29996935)
J Cell Physiol. 2015 Aug;230(8):1954-63. (PMID: 25612232)
Clin Cancer Res. 2011 Feb 15;17(4):700-9. (PMID: 21304002)
Biochem Biophys Res Commun. 2006 Jun 23;345(1):216-21. (PMID: 16678123)
Oncology. 2007;73(5-6):384-8. (PMID: 18511876)
Clin Cancer Res. 2003 Apr;9(4):1412-9. (PMID: 12684413)
Cell Commun Signal. 2017 Oct 3;15(1):38. (PMID: 28974231)
MedGenMed. 2004 Aug 13;6(3):13. (PMID: 15520636)
Oncogenesis. 2012 Jul 16;1:e20. (PMID: 23552736)
Oncotarget. 2016 Dec 27;7(52):86695-86703. (PMID: 27880730)
World J Gastroenterol. 2014 Dec 14;20(46):17376-87. (PMID: 25516649)
Breast Cancer Res. 2011 Jun 14;13(3):R63. (PMID: 21679465)
Nat Protoc. 2009;4(7):1073-81. (PMID: 19561590)
Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):543-52. (PMID: 18349271)
Grant Information :
801084 CAPES PROEX; 2013/08135-2 FAPESP; 12.1.25441.01.2./08135-2 CISBi-NAP/USP
Contributed Indexing :
Keywords: Adenocarcinoma; Adenoma; Colorectal; ETV4; Genetic markers
Substance Nomenclature :
0 (Biomarkers, Tumor)
0 (DNA, Neoplasm)
0 (ETV4 protein, human)
0 (Neoplasm Proteins)
0 (Proto-Oncogene Proteins c-ets)
0 (RNA, Small Interfering)
Entry Date(s) :
Date Created: 20210302 Date Completed: 20210430 Latest Revision: 20210430
Update Code :
20210623
PubMed Central ID :
PMC7919324
DOI :
10.1186/s12885-021-07857-x
PMID :
33648461
Czasopismo naukowe
Background: Colorectal cancer (CRC) is one of the most common cancers worldwide; it is the fourth leading cause of death in the world and the third in Brazil. Mutations in the APC, DCC, KRAS and TP53 genes have been associated with the progression of sporadic CRC, occurring at defined pathological stages of the tumor progression and consequently modulating several genes in the corresponding signaling pathways. Therefore, the identification of gene signatures that occur at each stage during the CRC progression is critical and can present an impact on the diagnosis and prognosis of the patient. In this study, our main goal was to determine these signatures, by evaluating the gene expression of paired colorectal adenoma and adenocarcinoma samples to identify novel genetic markers in association to the adenoma-adenocarcinoma stage transition.
Methods: Ten paired adenoma and adenocarcinoma colorectal samples were subjected to microarray gene expression analysis. In addition, mutations in APC, KRAS and TP53 genes were investigated by DNA sequencing in paired samples of adenoma, adenocarcinoma, normal tissue, and peripheral blood from ten patients.
Results: Gene expression analysis revealed a signature of 689 differentially expressed genes (DEG) (fold-change> 2, p< 0.05), between the adenoma and adenocarcinoma paired samples analyzed. Gene pathway analysis using the 689 DEG identified important cancer pathways such as remodeling of the extracellular matrix and epithelial-mesenchymal transition. Among these DEG, the ETV4 stood out as one of the most expressed in the adenocarcinoma samples, further confirmed in the adenocarcinoma set of samples from the TCGA database. Subsequent in vitro siRNA assays against ETV4 resulted in the decrease of cell proliferation, colony formation and cell migration in the HT29 and SW480 colorectal cell lines. DNA sequencing analysis revealed KRAS and TP53 gene pathogenic mutations, exclusively in the adenocarcinomas samples.
Conclusion: Our study identified a set of genes with high potential to be used as biomarkers in CRC, with a special emphasis on the ETV4 gene, which demonstrated involvement in proliferation and migration.

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