About this Research Topic
Stemness, metastasis and cancer recurrence are some of the key aspects of carcinogenesis which have been most intensely studied over the last ten years. In this regard, the metabolic aspects of the transformation process remain an area of great interest. A significant problem in cancer biology is to understand the precise role of the Epithelial-Mesenchymal Transition (EMT), which describes how epithelial cells gradually transform into mesenchymal-like cells, thereby losing their epithelial functionality and differentiated characteristics. It is known that dysregulation of metabolic processes is associated with early aspects of the EMT response; mitochondrial defects have a key role in cancer and in EMT induction. Consequences of mitochondrial dysfunction have been shown to be involved in tumorigenesis from tumour progression to metastasis. The observed alteration of metabolism compartments and mitochondrial functionality have been associated with numerous clinical outcomes across multiple cancer types and correlated with a specific EMT gene signature.
The EMT is thought to be involved in the pathogenesis of numerous human diseases, from various developmental disorders to cancer. An important open question and hotly debated topic is exactly how the EMT contributes to the pathogenesis of cancer, as well as tumor progression and metastasis. This Research topic will focus on studies that address these issues, starting from the normal developmental processes of cell growth to uncontrolled developmental processes, such as cancer. This area of Research broadly embraces cell biology, and in particular cancer biology, biochemistry, molecular biology and bioinformatics. This research topic will highlight the connections between metabolic processes and signal transduction pathways involved in the EMT process, as well as cancer stemness, in particular, studies of proteins and genes involved in oncogenic pathways and mitochondrial dysfunctions, the evaluation of metabolic cancer phenotypes, the reproduction of organs (3D organoids) in vitro and the use of new potential inhibitors of cancer stem cell biogenesis, which will allow for a better understanding of the molecular processes involved in stem cell self-renewal and tumor cell differentiation. Moreover, in vivo studies will also allow for a better mechanistic understanding of metastatic dissemination and the practical evaluation of new inhibitors or repurposed FDA approved drugs.
The scope of this Research topic is to better define changes in metabolic pathways in response to the EMT process and the role of mitochondria in cancer development and stemness. This Research Topic will focus on the latest advances in EMT process and mitochondrial metabolism research in the context of cancer and cancer metastasis. We welcome original research articles, as well as review articles including, but not strictly limited to:
• Metabolic reprogramming of cancer and stromal cells during cancer metastasis, including
bioenergetics, metabolic flux, carbohydrate, lipid, and amino acid metabolism.
• New potential inhibitors of the EMT process in cancer and new potential applications in the
therapeutic targeting of cancer and cancer metastasis.
• Metabolic phenotypes and mitochondrial functions in drug-resistant cancer cells.
• Metabolic abnormalities and metabolic changes in cancer metastasis driven by tumour-associated
genes, transcription factors and the mutation of regulatory protein, involved in metabolic pathways
and mitochondrial function.
• New biomarkers for epithelial-mesenchymal transition (EMT) and the mesenchymal-epithelial
transition (MET).
The EMT is thought to be involved in the pathogenesis of numerous human diseases, from various developmental disorders to cancer. An important open question and hotly debated topic is exactly how the EMT contributes to the pathogenesis of cancer, as well as tumor progression and metastasis. This Research topic will focus on studies that address these issues, starting from the normal developmental processes of cell growth to uncontrolled developmental processes, such as cancer. This area of Research broadly embraces cell biology, and in particular cancer biology, biochemistry, molecular biology and bioinformatics. This research topic will highlight the connections between metabolic processes and signal transduction pathways involved in the EMT process, as well as cancer stemness, in particular, studies of proteins and genes involved in oncogenic pathways and mitochondrial dysfunctions, the evaluation of metabolic cancer phenotypes, the reproduction of organs (3D organoids) in vitro and the use of new potential inhibitors of cancer stem cell biogenesis, which will allow for a better understanding of the molecular processes involved in stem cell self-renewal and tumor cell differentiation. Moreover, in vivo studies will also allow for a better mechanistic understanding of metastatic dissemination and the practical evaluation of new inhibitors or repurposed FDA approved drugs.
The scope of this Research topic is to better define changes in metabolic pathways in response to the EMT process and the role of mitochondria in cancer development and stemness. This Research Topic will focus on the latest advances in EMT process and mitochondrial metabolism research in the context of cancer and cancer metastasis. We welcome original research articles, as well as review articles including, but not strictly limited to:
• Metabolic reprogramming of cancer and stromal cells during cancer metastasis, including
bioenergetics, metabolic flux, carbohydrate, lipid, and amino acid metabolism.
• New potential inhibitors of the EMT process in cancer and new potential applications in the
therapeutic targeting of cancer and cancer metastasis.
• Metabolic phenotypes and mitochondrial functions in drug-resistant cancer cells.
• Metabolic abnormalities and metabolic changes in cancer metastasis driven by tumour-associated
genes, transcription factors and the mutation of regulatory protein, involved in metabolic pathways
and mitochondrial function.
• New biomarkers for epithelial-mesenchymal transition (EMT) and the mesenchymal-epithelial
transition (MET).
Keywords: EMT Process, CSCs, Mitochondria Metabolism, EMT Inhibitors, Metastasis
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
