TY - JOUR
T1 - Cross-talk between inflammatory mediators and the epithelial mesenchymal transition process in the development of thyroid carcinoma
AU - Revilla, Giovanna
AU - Corcoy, Rosa
AU - Moral, Antonio
AU - Escolà-Gil, Joan Carles
AU - Mato, Eugenia
PY - 2019/5/2
Y1 - 2019/5/2
N2 - © 2019 by the authors. Licensee MDPI, Basel, Switzerland. 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.
AB - © 2019 by the authors. Licensee MDPI, Basel, Switzerland. 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.
KW - Adiponectin
KW - High-density lipoproteins
KW - Leptin
KW - Low-density lipoproteins
KW - MET/EMT
KW - Signaling pathways
KW - Thyroid carcinoma
KW - Inflammation Mediators/metabolism
KW - Cell Proliferation
KW - Signal Transduction
KW - Humans
KW - Neoplastic Stem Cells/metabolism
KW - Lipoproteins, LDL/metabolism
KW - Cell Transformation, Neoplastic/metabolism
KW - Lipoproteins, HDL/metabolism
KW - Animals
KW - Epithelial-Mesenchymal Transition
KW - Biomarkers
KW - Cell Line, Tumor
KW - Cell Differentiation
KW - Thyroid Neoplasms/etiology
KW - Mutation
UR - http://www.mendeley.com/research/crosstalk-between-inflammatory-mediators-epithelial-mesenchymal-transition-process-development-thyro
U2 - 10.3390/ijms20102466
DO - 10.3390/ijms20102466
M3 - Review article
C2 - 31109060
SN - 1661-6596
VL - 20
JO - International journal of molecular sciences
JF - International journal of molecular sciences
IS - 10
M1 - 2466
ER -