MiR-205 functions as a tumor suppressor in adenocarcinoma and an oncogene in squamous cell carcinoma of esophagus
Language English Country United States Media print-electronic
Document type Journal Article
PubMed
26711784
DOI
10.1007/s13277-015-4656-8
PII: 10.1007/s13277-015-4656-8
Knihovny.cz E-resources
- Keywords
- Esophageal adenocarcinoma, Esophageal squamous cell carcinoma, Oncogene, Tumor suppressor, miR-205,
- MeSH
- Adenocarcinoma genetics metabolism pathology MeSH
- Apoptosis genetics MeSH
- Cell Cycle genetics MeSH
- Adult MeSH
- Epithelial-Mesenchymal Transition genetics MeSH
- Real-Time Polymerase Chain Reaction MeSH
- Middle Aged MeSH
- Humans MeSH
- MicroRNAs physiology MeSH
- Survival Rate MeSH
- Cell Line, Tumor MeSH
- Esophageal Neoplasms genetics metabolism pathology MeSH
- Oncogenes genetics MeSH
- Cell Movement genetics MeSH
- Cell Proliferation genetics MeSH
- Gene Expression Regulation, Neoplastic physiology MeSH
- Aged MeSH
- Esophageal Squamous Cell Carcinoma MeSH
- Carcinoma, Squamous Cell genetics metabolism pathology MeSH
- Gene Expression Profiling MeSH
- Genes, Tumor Suppressor MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- MicroRNAs MeSH
- MIRN205 microRNA, human MeSH Browser
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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