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Submitted on March 30, 2006
Accepted on June 28, 2006
Genomic Medicine Institute (F.W., R.E.T, C.E), Lerner Research Institute and Taussig Cancer Center (C.E.), Cleveland Clinic Foundation, Cleveland, OH; Department of General Surgery and Transplantation, University Hospital of Essen, Essen, Germany (F.W., C.E.B, A.F); Department of Genetics (C.E.) and CASE Comprehensive Cancer Center (C.E.), Case Western Reserve University School of Medicine, Cleveland, OH
* To whom correspondence should be addressed. E-mail: engc{at}ccf.org.
Context: While the pathogenesis of follicular thyroid carcinoma (FTC) and its relation to follicular adenoma (FA) remains unclear, detailed understanding of FTC carcinogenesis would facilitate addressing the scientific and clinical challenges given that there are morphological and molecular similarities between FTC and the frequently occurring FA. Micro-RNA's (miRNA's) are a new class of small, non-coding RNA's implicated in development and cancer, and may lend novel clues to FTC genesis. For the latter process, a deregulated miRNA can orchestrate the aberrant expression of several hundred target genes.
Objective: To identify deregulated micro-RNA's in follicular thyroid cancer.
Design: We used two high-density expression arrays to identify miRNA's and their target genes that are differentially expressed between FTC and FA. Validation was done by qRT-PCR. We further functionally characterized the effect of deregulated miRNAs in vitro using HEK293T, FTC133 and K5 cell lines.
Patients: In total, 45 primary thyroid samples (23 FTC, 20 FA, 4 normal control thyroid) were analyzed.
Results: Two specific miRNA's, miR-197 and miR-346, were significantly over-expressed in FTC. In vitro over-expression of either miRNA induced proliferation, while inhibition led to growth arrest. Over-expression of miR-197 and miR-346 repressed the expression of their predicted target genes in vitro and in vivo.
Conclusions: Our observations show that miR-197 and miR-346 contribute to FTC carcinogenesis. Both miRNA's and their target genes might potentially provide for novel molecular markers and act as novel targets for treatment by interference, which could potentially normalize the deregulated profile of many downstream target genes.
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