Journal
ONCOLOGY LETTERS
Volume 17, Issue 1, Pages 1080-1088Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2018.9692
Keywords
canine melanoma; microRNA; microarray; oncomiR; microRNA-target regulatory interaction network
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Funding
- Japan Society for the Promotion of Science KAKENHI [17H03926, 15H14872, 25292180, 22780283]
- Grants-in-Aid for Scientific Research [22780283] Funding Source: KAKEN
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Inhibiting aberrantly upregulated microRNAs (miR/miRNAs) has emerged as a novel focus for therapeutic intervention in human melanoma. Thus, identifying upregulated miRNAs is essential for identifying additional melanoma-associated therapeutic targets. In the present study, microarray-based miRNA profiling of canine malignant melanoma (CMM) tissue obtained from the oral cavity was performed and differential expression was confirmed by a reverse transcription-quantitative polymerase chain reaction (RT-qPCR). An analysis of the microarray data revealed 17 dysregulated miRNAs; 5 were upregulated and 12 were downregulated. RT-qPCR analysis was performed for 2 upregulated (miR-204 and miR-383), 3 downregulated (miR-122, miR-143 and miR-205) and 6 additional oncogenic miRNAs (oncomiRs; miR-16, miR-21, miR-29b, miR-92a, miR-125b and miR-222). The expression levels of seven of the miRNAs, miR-16, miR-21, miR-29b, miR-122, miR-125b, miR-204 and miR-383 were significantly upregulated; however, the expression of miR-205 was downregulated in CMM tissues compared with normal oral tissues. The microarray and RT-qPCR analyses validated the upregulation of two potential oncomiRs miR-204 and miR-383. The present study additionally constructed a protein interaction network and a miRNA-target regulatory interaction network using STRING and Cytoscape. In the proposed network, cyclin dependent kinase 2 was a target for miR-383, sirtuin 1 and tumor protein p53 were targets for miR-204 and ATR serine/threonine kinase was a target for both. It was concluded that miR-383 and miR-204 were potential oncomiRs that may be involved in regulating melanoma development by evading DNA repair and apoptosis.
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