Open AccessMicroRNA Profiling of Salivary Adenoid Cystic Carcinoma: Association of miR-17-92 Upregulation with Poor Outcome
Author(s) -
Yoshitsugu Mitani,
Dianna B. Roberts,
Hanadi Fatani,
Randal S. Weber,
Merrill S. Kies,
Scott M. Lippman,
Adel K. ElNaggar
Publication year - 2013
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0066778
Subject(s) - carcinogenesis , adenoid cystic carcinoma , microrna , downregulation and upregulation , biology , mir 155 , cancer research , myb , pathology , oncology , carcinoma , cancer , bioinformatics , medicine , gene expression , genetics , gene
Background Salivary adenoid cystic carcinoma (ACC) is a rare relentlessly progressive malignant tumor. The molecular events associated with ACC tumorigenesis are poorly understood. Variable microRNAs (miRNA) have been correlated with tumorigenesis of several solid tumors but not in ACC. To investigate the association of miRNAs with the development and/or progression of ACC, we performed a comparative analysis of primary ACC specimens and matched normal samples and a pooled salivary gland standard and correlated the results with clinicopathologic factors and validated selected miRNAs in a separate set of 30 tumors. Methods MiRNA array platform was used for the identification of target miRNAs and the data was subjected to informatics and statistical interrelations. The results were also collected with the MYB-NFIB fusion status and the clinicopathologic features. Results Differentially dysregulated miRNAs in ACC were characterized in comparison to normal expression. No significant differences in miRNA expression were found between the MYB-NFIB fusion positive and -negative ACCs. Of the highly dysregulated miRNA in ACC, overexpression of the miR-17 and miR-20a were significantly associated with poor outcome in the screening and validation sets. Conclusion Our study indicates that the upregulation of miR-17-92 may play a role in the biology of ACC and could be potentially targeted in future therapeutic studies.