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International Journal of Endocrinology
Volume 2015 (2015), Article ID 439370, 11 pages
Research Article

Anaplastic Thyroid Carcinoma: A ceRNA Analysis Pointed to a Crosstalk between SOX2, TP53, and microRNA Biogenesis

1Section of Cardio-Respiratory and Endocrine-Metabolic Diseases, Biomedical Department of Internal and Specialist Medicine (Di.Bi.M.I.S.), University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy
2Istituto Ortopedico Rizzoli (IOR), Section of Biology and Genetics, Department of Pathobiology and Medical and Forensic Biotechnology (Di.Bi.Me.F.), University of Palermo, Via Divisi 83, 90100 Palermo, Italy

Received 30 May 2014; Revised 28 August 2014; Accepted 10 September 2014

Academic Editor: Giuliana Salvatore

Copyright © 2015 Walter Arancio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It has been suggested that cancer stem cells (CSC) may play a central role in oncogenesis, especially in undifferentiated tumours. Anaplastic thyroid carcinoma (ATC) has characteristics suggestive of a tumour enriched in CSC. Previous studies suggested that the stem cell factor SOX2 has a preeminent hierarchical role in determining the characteristics of stem cells in SW1736 ATC cell line. In detail, silencing SOX2 in SW1736 is able to suppress the expression of the stem markers analysed, strongly sensitizing the line to treatment with chemotherapeutic agents. Therefore, in order to further investigate the role of SOX2 in ATC, a competing endogenous RNA (ceRNA) analysis was conducted in order to isolate new functional partners of SOX2. Among the interactors, of particular interest are genes involved in the biogenesis of miRNAs (DICER1, RNASEN, and EIF2C2), in the control cell cycle (TP53, CCND1), and in mitochondrial activity (COX8A). The data suggest that stemness, microRNA biogenesis and functions, p53 regulatory network, cyclin D1, and cell cycle control, together with mitochondrial activity, might be coregulated.