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Updated: Jan 21, 2026

Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
Epithelial-to-mesenchymal transition in thyroid cancer: a comprehensive review
Heewa Shakib1, Sadegh Rajabi2, Mohammad Hossien Dehghan3
1Cellular and Molecular Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
The Metastatic progression of solid tumors, such as thyroid cancer is a complex process which involves various factors. Current understanding on the role of epithelial-mesenchymal transition (EMT) in thyroid carcinomas suggests that EMT is implicated in the progression from follicular thyroid cancer (FTC) and papillary thyroid cancer (PTC) to poorly differentiated thyroid carcinoma (PDTC) and anaplastic thyroid cancer (ATC). According to the literature, the initiation of the EMT program in thyroid epithelial cells elevates the number of stem cells, which contribute to recurrent and metastatic diseases. The EMT process is orchestrated by a complex network of transcription factors, growth factors, signaling cascades, epigenetic modulations, and the tumor milieu. These factors have been shown to be dysregulated in thyroid carcinomas. Therefore, molecular interferences restoring the expression of tumor suppressors, or thwarting overexpressed oncogenes is a hopeful therapeutic method to improve the treatment of progressive diseases. In this review, we summarize the recent findings on EMT in thyroid cancer focusing on the main role-players and regulators of this process in thyroid tumors.
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