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SHR Neuro Krebs Kardio Lipid

Pehserl, AM; Ress, AL; Stanzer, S; Resel, M; Karbiener, M; Stadelmeyer, E; Stiegelbauer, V; Gerger, A; Mayr, C; Scheideler, M; Hutterer, GC; Bauernhofer, T; Kiesslich, T; Pichler, M.
Comprehensive Analysis of miRNome Alterations in Response to Sorafenib Treatment in Colorectal Cancer Cells.
Int J Mol Sci. 2016; 17(12): [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Autor/innen der Med Uni Graz:
Bauernhofer Thomas
Gerger Armin
Hutterer Georg C.
Karbiener Michael
Lembeck Anna Lena
Pehserl Anna-Maria
Pichler Martin
Resel Margit
Stadelmeyer Elke
Stanzer Stefanie
Stiegelbauer Verena
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Number of Figures: 5
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Abstract:
MicroRNAs (miRNAs) are master regulators of drug resistance and have been previously proposed as potential biomarkers for the prediction of therapeutic response in colorectal cancer (CRC). Sorafenib, a multi-kinase inhibitor which has been approved for the treatment of liver, renal and thyroid cancer, is currently being studied as a monotherapy in selected molecular subtypes or in combination with other drugs in metastatic CRC. In this study, we explored sorafenib-induced cellular effects in Kirsten rat sarcoma viral oncogene homolog olog (KRAS) wild-type and KRAS-mutated CRC cell lines (Caco-2 and HRT-18), and finally profiled expression changes of specific miRNAs within the miRNome (>1000 human miRNAs) after exposure to sorafenib. Overall, sorafenib induced a time- and dose-dependent growth-inhibitory effect through S-phase cell cycle arrest in KRAS wild-type and KRAS-mutated CRC cells. In HRT-18 cells, two human miRNAs (hsa-miR-597 and hsa-miR-720) and two small RNAs (SNORD 13 and hsa-miR-3182) were identified as specifically sorafenib-induced. In Caco-2 cells, nine human miRNAs (hsa-miR-3142, hsa-miR-20a, hsa-miR-4301, hsa-miR-1290, hsa-miR-4286, hsa-miR-3182, hsa-miR-3142, hsa-miR-1246 and hsa-miR-720) were identified to be differentially regulated post sorafenib treatment. In conclusion, we confirmed sorafenib as a potential anti-neoplastic treatment strategy for CRC cells by demonstrating a growth-inhibitory and cell cycle-arresting effect of this drug. Changes in the miRNome indicate that some specific miRNAs might be relevant as indicators for sorafenib response, drug resistance and potential targets for combinatorial miRNA-based drug strategies.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Caco-2 Cells -
Cell Cycle Checkpoints - drug effects
Colorectal Neoplasms - drug therapy
Colorectal Neoplasms - genetics
Colorectal Neoplasms - pathology
Drug Resistance, Neoplasm - genetics
Gene Expression Regulation, Neoplastic -
Humans -
MicroRNAs - biosynthesis
MicroRNAs - genetics
Mutation -
Niacinamide - administration & dosage
Niacinamide - analogs & derivatives
Phenylurea Compounds - administration & dosage
Proto-Oncogene Proteins p21(ras) - genetics
Sorafenib -

Find related publications in this database (Keywords)
colorectal cancer
sorafenib
miRNA
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