Osteopontin Expression in Thyroid Cancer: Deciphering EMT-Related Molecular Mechanisms

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.

Automated summary

Thyroid cancer, the most common tumor arising from the endocrine system, typically has a good prognosis, but aggressive subtypes can be resistant to therapy and lead to early metastasis. Epithelial-mesenchymal transition and its reverse, mesenchymal-epithelial transition, play key roles in cancer progression, including in thyroid cancer. Although the matricellular protein osteopontin is known to regulate EMT in various tumor types, its specific role in thyroid cancer has not been definitively established.