Journal
JOURNAL OF ORAL PATHOLOGY & MEDICINE
Volume 45, Issue 4, Pages 248-255Publisher
WILEY-BLACKWELL
DOI: 10.1111/jop.12351
Keywords
epithelial mesenchymal transition; metastasis; microRNA; miR-155; oral cancer
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Funding
- JSPS KAKENHI [25893024]
- Grants-in-Aid for Scientific Research [15K15318, 25893024, 25293125, 15H05038] Funding Source: KAKEN
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BackgroundAbnormal miRNA expression was recently implicated in the metastasis of oral squamous cell carcinoma (OSCC) and with a poor prognosis. The initiation of the invasion-metastasis cascade involves epithelial-mesenchymal transition (EMT). Our aim was to clarify how miRNA, especially miR-155-5p misexpression contributes to OSCC metastasis through EMT. MethodsWe collected tumor samples from 73 subjects with OSCC. The samples were analyzed by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and correlations between miR-155-5p levels and clinical characteristics were investigated. OSCC cell lines were analyzed by miRNA microarray and by transfection with a miR-155-5p mimic or inhibitor, followed by proliferation and wound-healing migration assays. qRT-PCR analyses of EMT makers in cells transfected with miR-155-5p inhibitor were performed. ResultsWe found high miR-155-5p expression in tissue samples from subjects with OSCC that had metastasized to cervical lymph nodes. HSC-3 cells also strongly expressed miR-155-5p. The epithelial marker E-cadherin was strongly expressed in HSC-3 cells transfected with miR-155-5p inhibitor, and we observed elevated SOCS1 and decreased STAT3 expression in these cells. ConclusionsOur results suggest that miR-155-5p causes OSCC to metastasize, and could serve as a novel therapeutic target for OSCC.
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