ECE2015 Eposter Presentations Thyroid cancer (90 abstracts)
Role of miR-26a in follicular thyroid carcinoma
Erica Gentilin 1, , Elisa Ortolan 1 , Teresa Gagliano 1 , Carmelina Di Pasquale 1 , Simona Falletta 1 , Roberta Rossi 1 , Katiuscia Benfini 1 , Federico Tagliati 1 , Ettore Degli Uberti 1, & Maria Chiara Zatelli 1,
1Department of Medical Sciences, University of Ferrara, Ferrara, Italy; 2LTTA, Laboratorio per le Tecnologie delle Terapie Avanzate, Ferrara, Italy.
Follicular thyroid carcinoma (FTC) is the second most common thyroid malignant epithelial tumor. It is clinically asymptomatic, usually represented by a single nodule, less often multiple, with origin from thyroid follicular epithelial cells. Despite its well-differentiated characteristics, FTC may develop distant metastases through hematogenous dissemination. The molecular alterations involved in the pathogenesis of follicular neoplasia are not completely known. Recent studies have demonstrated the importance of miRNAs, small non-coding nucleic acids that regulate gene expression at post-transcriptional level. It is well known that the expression profile of miRNAs is altered in follicular thyroid carcinoma. To date, the aftermaths of deregulated expression of miRNAs in the FTC have not been clarified. In order to investigate the molecular mechanisms involved in thyroid tumorigenesis, we evaluated the effects of miR-26a modulation in a human FTC cell line. We observed that miR-26a is significantly down-regulated in FTC-133 cells as compared to a thyroid normal cell line, NTHY-ORI. Our results demonstrated that miR-26a does not directly regulate Protein Kinsae C Delta (PRKCD), a known target of this miRNA, but influences its levels. PRKCD is a regulator of caspase-mediated apoptosis, vascular endothelial growth factor (VEGF)-mediated cell proliferation and iodide uptake via sodium iodide symporter (NIS). We observed that miR-26a up-regulation increases PRKCD and NIS protein levels as well as caspase activity, but does not influence VEGF secretion. These results support the hypothesis that miR-26a may influence thyroid differentiation processes and nay represent a therapeutic target for future innovative therapy in advanced radio-refractory disease.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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