Anaplastic thyroid cancer (ATC) is among the most lethal types of
cancers, characterized as a fast-growing and highly invasive thyroid
tumor that is unresponsive to surgery and radioiodine, blunting therapeutic efficacy. Classically, genetic alterations in
tumor suppressor TP53 are frequent, and cumulative alterations in different signaling pathways, such as MAPK and PI3K, are detected in ATC. Recently, deregulation in
microRNAs (
miRNAs), a class of small endogenous RNAs that regulate
protein expression, has been implicated in
tumorigenesis and
cancer progression. Deregulation of
miRNA expression is detected in
thyroid cancer. Upregulation of
miRNAs, such as miR-146b, miR-221, and miR-222, is observed in ATC and also in differentiated
thyroid cancer (papillary and follicular), indicating that these
miRNAs' overexpression is essential in maintaining
tumorigenesis. However, specific
miRNAs are downregulated in ATC, such as those of the miR-200 and miR-30 families, which are important negative regulators of cell migration, invasion, and epithelial-to-mesenchymal transition (EMT), processes that are overactivated in ATC. Therefore, molecular interference to restore the expression of
tumor suppressor
miRNAs, or to blunt overexpressed oncogenic
miRNAs, is a promising therapeutic approach to ameliorate the treatment of ATC. In this review, we will explore the importance of
miRNA deregulation for ATC cell biology.