Abstract
Thyroid cancer is the most common tumor arising from the endocrine system and generally presents good prognosis. However, its aggressive subtypes are related to therapeutic resistance and early metastasis. Epithelial–mesenchymal transition (EMT) and its reverse process, the mesenchymal–epithelial transition (MET), are key events mediating cancer progression, including in thyroid cancer. The matricellular protein osteopontin (OPN) has been reported as a master regulator of EMT in many tumor types. Although high OPN expression has been described and associated with important aspects of thyroid cancer progression, there is no clear evidence regarding OPN as a regulator of EMT in thyroid cancer. Thus, taking together the known roles of OPN in the modulation of EMT in cancer and the information reporting the expression of OPN in thyroid tumor progression, this review aims at summarizing and discussing data related to EMT in thyroid cancer and its putative relation to the roles of OPN in the development of thyroid cancer. These data provide new insights into the molecular mechanisms by which OPN could potentially modulate EMT in thyroid tumors, generating evidence for future studies that may contribute to new therapeutic, prognostic and/or diagnostic tools.
Highlights
Thyroid tumors are the most common malignancies of the endocrine system, representing the fifth most prevalent cancer worldwide [1]
ZEB1 is a transcription factor that is related to the activation of Epithelial–mesenchymal transition (EMT) with outstanding expression in thyroid tumors, with this being related to the occurrence of metastasis as well as cell migration, invasion and proliferation in anaplastic and in medullary thyroid carcinoma cell lines [49]
Given the overexpression of osteopontin in thyroid cancer cells and its known association with several events that are generally associated with EMT in thyroid tumors, these data further reinforce the notion that OPN is a master regulator of epithelial mesenchymal plasticity in thyroid cancer
Summary
Thyroid tumors are the most common malignancies of the endocrine system, representing the fifth most prevalent cancer worldwide [1]. Biomedicines 2021, 9, 1372 colonize and develop the different embryonic leaflets, in addition to organ formation [3] This process is well described during the development of cancer, in which tumor cells often lose their epithelial phenotype while mesenchymal markers are upregulated, favoring higher migration, invasion and metastasis rates. This review aims at shedding light on the current knowledge related to EMT in thyroid tumors and the pivotal contribution of OPN as an EMT modulator in different tumor types Considering these data, we focus on describing and discussing the putative relationship of OPN as a potential EMT regulator in the development of thyroid cancer, providing new clues regarding the molecular mechanisms by which OPN could modulate epithelial–mesenchymal plasticity in this tumor type, possibly generating evidence that can contribute towards the future development of new therapeutic, prognostic and/or diagnostic tools
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