MiR-205 functions as a tumor suppressor in adenocarcinoma and an oncogene in squamous cell carcinoma of esophagus
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články
PubMed
26711784
DOI
10.1007/s13277-015-4656-8
PII: 10.1007/s13277-015-4656-8
Knihovny.cz E-zdroje
- Klíčová slova
- Esophageal adenocarcinoma, Esophageal squamous cell carcinoma, Oncogene, Tumor suppressor, miR-205,
- MeSH
- adenokarcinom genetika metabolismus patologie MeSH
- apoptóza genetika MeSH
- buněčný cyklus genetika MeSH
- dospělí MeSH
- epitelo-mezenchymální tranzice genetika MeSH
- kvantitativní polymerázová řetězová reakce MeSH
- lidé středního věku MeSH
- lidé MeSH
- mikro RNA fyziologie MeSH
- míra přežití MeSH
- nádorové buněčné linie MeSH
- nádory jícnu genetika metabolismus patologie MeSH
- onkogeny genetika MeSH
- pohyb buněk genetika MeSH
- proliferace buněk genetika MeSH
- regulace genové exprese u nádorů fyziologie MeSH
- senioři MeSH
- skvamózní karcinom jícnu MeSH
- spinocelulární karcinom genetika metabolismus patologie MeSH
- stanovení celkové genové exprese MeSH
- tumor supresorové geny MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- mikro RNA MeSH
- MIRN205 microRNA, human MeSH Prohlížeč
Esophageal cancer is a malignant disease with poor prognosis, increasing incidence, and ineffective treatment options. MicroRNAs are post-transcriptional regulators of gene expression involved in many biological processes including carcinogenesis. We determined miR-205 expression levels in tumor/non-tumor tissues of 45 esophageal cancer patients using qPCR and found that decreased level of miR-205 in tumor tissue correlates with poor overall survival in esophageal adenocarcinoma patients. Further, we observed significantly higher levels of miR-205 in tumor tissue of esophageal squamous cell carcinoma. Ectopic overexpression of miR-205 in adenocarcinoma cell line SK-GT-4 led to decreased cell proliferation, cell cycle arrest in G1, and decreased migration ability. Conversely, in squamous cell line KYSE-150, same effects like inhibition of proliferation, migration, and colony-forming potential and cell cycle arrest in G2 were observed after silencing of miR-205. We performed global gene expression profiling and revealed that suppressive functioning of miR-205 in adenocarcinoma could be realized through regulation of epithelial-mesenchymal transition (EMT), whereas oncogenic in squamous cell carcinoma by regulation of metalloproteinase 10. Our results suggest that miR-205 could serve as biomarker in esophageal cancer and acts as a tumor suppressor in esophageal adenocarcinoma and oncogene in esophageal squamous cell carcinoma.
Central European Institute of Technology Masaryk University Brno Czech Republic
Central European Institute of Technology Masaryk University Kamenice 5 Brno 625 00 Czech Republic
Department of Comprehensive Cancer Care Masaryk Memorial Cancer Institute Brno Czech Republic
Department of Surgery University Hospital in Motol Praha Czech Republic
Olomouc Faculty of Medicine Palacky University Olomouc Czech Republic
Oncology Department General University Hospital Prague Praha Czech Republic
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Int J Cancer. 2013 Jun 15;132(12):2884-93 PubMed
J Clin Oncol. 2007 Aug 20;25(24):3719-25 PubMed
Clin Chem. 2014 Jan;60(1):197-205 PubMed
Cancer Cell. 2006 Mar;9(3):189-98 PubMed
Hematol Oncol Clin North Am. 2010 Oct;24(5):815-35 PubMed
Br J Cancer. 2012 Jan 31;106(3):553-61 PubMed
Onco Targets Ther. 2014 Jun 18;7:1083-94 PubMed
Oncol Res Treat. 2014;37(11):658-64 PubMed
J Clin Invest. 2014 Jul;124(7):3093-106 PubMed
Cancer Res. 2009 Mar 15;69(6):2287-95 PubMed
Mol Biol Cell. 2012 Oct;23(19):3873-81 PubMed
PLoS One. 2013 Oct 02;8(10):e76402 PubMed
Oncol Rep. 2013 Dec;30(6):2897-902 PubMed
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 PubMed
Biochem Biophys Res Commun. 2013 Nov 8;441(1):139-43 PubMed
Nature. 2005 Jun 9;435(7043):834-8 PubMed
Oncol Rep. 2013 Jun;29(6):2297-302 PubMed
Br J Cancer. 2013 Apr 30;108(8):1668-76 PubMed
Asian Pac J Cancer Prev. 2013;14(1):139-43 PubMed
J Cell Sci. 2010 Feb 15;123(Pt 4):606-18 PubMed
Oncol Rep. 2010 Jun;23(6):1625-33 PubMed
Cancer Res. 2011 Apr 1;71(7):2611-21 PubMed
Tumour Biol. 2013 Feb;34(1):481-91 PubMed
Clin Cancer Res. 2014 Dec 15;20(24):6324-35 PubMed
Int J Cancer. 2011 Mar 15;128(6):1327-34 PubMed
Asian Pac J Cancer Prev. 2014;15(2):577-83 PubMed
Clin Transl Gastroenterol. 2013 May 16;4:e34 PubMed
Eur Rev Med Pharmacol Sci. 2014 Oct;18(19):2783-8 PubMed
Int J Cancer. 2009 Mar 15;124(6):1358-65 PubMed
J Breast Cancer. 2014 Jun;17(2):143-8 PubMed
N Engl J Med. 2012 May 31;366(22):2074-84 PubMed
J Clin Oncol. 2009 Oct 20;27(30):5062-7 PubMed
PLoS One. 2010 Sep 30;5(9):null PubMed
PLoS One. 2013 May 28;8(5):e64463 PubMed
Nat Cell Biol. 2008 May;10 (5):593-601 PubMed
Cancer Prev Res (Phila). 2013 Mar;6(3):196-205 PubMed
Dev Biol. 2007 Feb 1;302(1):1-12 PubMed
Semin Oncol. 1994 Aug;21(4):403-10 PubMed
J Biol Chem. 2011 May 13;286(19):16606-14 PubMed
BMC Med Genomics. 2012 May 29;5:18 PubMed
J Transl Med. 2011 Mar 22;9:30 PubMed
CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 PubMed
Bioinformatics. 2010 Oct 1;26(19):2363-7 PubMed
Med Oncol. 2014 Jan;31(1):785 PubMed
RNA. 2004 Nov;10(11):1813-9 PubMed
Cancer Res. 2013 Sep 1;73(17 ):5402-15 PubMed
Proc Natl Acad Sci U S A. 2008 Dec 9;105(49):19300-5 PubMed
