Metastasis is a multistep process during which secondary tumors are formed in distant organs. The first step of a metastatic cascade is the epithelial-mesenchymal transition (EMT). EMT requires complex expression… Click to show full abstract
Metastasis is a multistep process during which secondary tumors are formed in distant organs. The first step of a metastatic cascade is the epithelial-mesenchymal transition (EMT). EMT requires complex expression changes leading to the transformation of epithelial cells into mesenchymal ones, able to migrate. The changes in gene expression are brought about by a battery of well-characterized EMT-related transcription factors (EMT-TFs), responsible for the exchange of E-type cadherin into N-type cadherin, with a clearly defined role in promoting metastasis. The Research Topic “Role of Metabolic Remodeling in Cancer-Associated Epithelial-Mesenchymal Transition” aimed to gather information on metabolic features accompanying EMT, because conclusive information about cancer metabolic status in EMT is still rather elusive. In general, metabolic remodeling is a “support tool” for the survival of cancer cells and successful progression. Our extensive knowledge and methodological advances in the field of cancer metabolism are now being continuously applied to discover specificities of other dynamic cancer-related processes, such as EMT. Apparently, an in vitro link between metabolic and mesenchymal phenotype is reciprocal; specific mesenchymal markers might be associated with the specific expression pattern of metabolic genes, and vice-versa, changes to the expression of some metabolic enzymes induce or inhibit EMT, respectively. Metabolic processes supporting EMT are similar to the general principles in cancer metabolism studied so far, i.e.metabolic signaling towards epigenetics, regulating cofactor abundance, or supporting metabolic plasticity of cancer cells. Our article collection intended to point out relevant molecular links between the EMT process and specific metabolic enzymes or pathways. As stated above there are some links between a genetic and metabolic fragment of EMT influencing each other. A review by Georgakopoulos-Soares et al. wraps up information regarding the role of EMT-TFs in EMT and metabolic remodeling, and provides examples of how EMT-TFs possibly regulate metabolism. The authors summarize the consequences of EMT-TFs activity (Snail, Twist, and ZEB family) in EMT as well as in metabolism.
               
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