Abstract
There is strong association between inflammatory processes and their main metabolic mediators, such as leptin, adiponectin secretion, and low/high-density lipoproteins, with the cancer risk and aggressive behavior of solid tumors. In this scenario, cancer cells (CCs) and cancer stem cells (CSCs) have important roles. These cellular populations, which come from differentiated cells and progenitor stem cells, have increased metabolic requirements when it comes to maintaining or expanding the tumors, and they serve as links to some inflammatory mediators. Although the molecular mechanisms that are involved in these associations remain unclear, the two following cellular pathways have been suggested: 1) the mesenchymal-epithelial transition (MET) process, which permits the differentiation of adult stem cells throughout the acquisition of cell polarity and the adhesion to epithelia, as well to new cellular lineages (CSCs); and, 2) a reverse process, termed the epithelial-mesenchymal transition (EMT), where, in pathophysiological conditions (tissue injury, inflammatory process, and oxidative stress), the differentiated cells can acquire a multipotent stem cell-like phenotype. The molecular mechanisms that regulate both EMT and MET are complex and poorly understood. Especially, in the thyroid gland, little is known regarding MET/EMT and the role of CCs or CSCs, providing an exciting, new area of knowledge to be investigated. This article reviews the progress to date in research on the role of inflammatory mediators and metabolic reprogramming during the carcinogenesis process of the thyroid gland and the EMT pathways.
Highlights
Epithelial thyroid cancer (ETC) is the most common malignancy of the endocrine system, which affects the follicular cells of the gland
Papillary thyroid cancer (PTC) comprises about 85% of cases when compared with about 10%, which have follicular histology, referred to as follicular thyroid cancer (FTC), and 3–5% of the type FTC correspond to the Hürthle cell or oxyphil tumors characteristic
There are few studies regarding the relationship between leptin and the epithelial mesenchymal transition (EMT) process, but some reports have demonstrated that treatment with leptin can promote cell growth and modulated migration of Cancer Cells (CCs), as well as inhibiting apoptosis through of the upregulation of the XIAP gene [76]
Summary
Epithelial thyroid cancer (ETC) is the most common malignancy of the endocrine system, which affects the follicular cells of the gland. Sci. 2019, 20, 2466 than half of the diagnosed cases originate from well-differentiated tumors and represent 1–2% of all thyroid malignancies [9] These tumoral cells show and aggressive behaviour with a rapid grow, and in most of cases at the moment of diagnosis, the patients show local (lymph nodes) and distant metastasis (pulmonary). It is of note that only 10% of these tumors are resectable at the time of diagnosis and 131I therapy does not work, because they lack the typical differentiation feature of the thyroid gland (iodine uptake, thyroglobulin secretion, response to TSH stimulation) and are the most aggressive For that reason, they have a poor prognosis with a low survival within 6–12 months [10]
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