Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Ress, AL; Stiegelbauer, V; Winter, E; Schwarzenbacher, D; Kiesslich, T; Lax, S; Jahn, S; Deutsch, A; Bauernhofer, T; Ling, H; Samonigg, H; Gerger, A; Hoefler, G; Pichler, M.
MiR-96-5p influences cellular growth and is associated with poor survival in colorectal cancer patients.
Mol Carcinog. 2015; 54(11):1442-1450
Doi: 10.1002/mc.22218
Web of Science
PubMed
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FullText_MUG
- Führende Autor*innen der Med Uni Graz
- Lembeck Anna Lena
- Pichler Martin
- Co-Autor*innen der Med Uni Graz
- Bauernhofer Thomas
- Deutsch Alexander
- Gerger Armin
- Höfler Gerald
- Jahn Stephan
- Ninaus Daniela
- Samonigg Hellmut
- Stiegelbauer Verena
- Winter Elke
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- Abstract:
- Expression of miR-96-5p is frequently altered in various types of cancer and the KRAS oncogene has been identified as one of its potential targets. However, the biological role of miR-96-5p expression in colorectal cancer (CRC) and its ability to predict the clinical course of patients have not been investigated yet. In this study, we explored miR-96-5p expression in 80 CRC patients and evaluated the impact on clinical outcome by Kaplan-Meier curves and multivariate Cox proportional models. In vitro miR-96-5p inhibition and overexpression were performed in CRC cells and the effects on cellular growth, anchorage-independent growth, apoptosis, and epithelial-mesenchymal transition (EMT)-related gene expression were explored. Low miR-96-5p expression levels in tumor tissue were associated with distant metastasis (P = 0.025) and multivariate Cox regression analysis identified low levels of miR-96-5p as an independent prognostic factor with respect to cancer-specific survival (hazard ratio = 1.78, 95%CI = 1.03-3.03, P < 0.038). In vitro overexpression of miR-96-5p led to a reduced cellular growth rate (P < 0.05), reduced colonies in soft agar (P < 0.05), corroborated by a decreased cyclin D1 and increased p27-CDKN1A expression (P < 0.05). Forced expression of miR-96-5p in CRC cells entailed no effects on apoptosis or EMT-related genes but decreased the expression levels of the KRAS oncogene (P < 0.05). Despite regulating KRAS expression, there was no significant association in miR-96-5p expression levels and response rates to EGFR-targeting agents. In conclusion, our data suggest that miR-96-5p influences cellular growth of CRC cells and low expression of miR-96-5p seems to be associated with poor clinical outcome in CRC patients. © 2014 Wiley Periodicals, Inc.
- Find related publications in this database (using NLM MeSH Indexing)
- Apoptosis - genetics
- Cell Proliferation - genetics
- Colorectal Neoplasms - genetics
- Colorectal Neoplasms - mortality
- Cyclin-Dependent Kinase Inhibitor p21 - genetics
- Cyclin-Dependent Kinase Inhibitor p27 - genetics
- Epithelial-Mesenchymal Transition - genetics
- Female -
- Gene Expression Regulation, Neoplastic - genetics
- Genes, ras - genetics
- Humans -
- Male -
- MicroRNAs - genetics
- Middle Aged -
- Prognosis -
- Proportional Hazards Models -
- Find related publications in this database (Keywords)
- colorectal cancer
- microRNAs
- prognosis