Cancer cells use a variety of metabolic reprogramming strategies to survive and proliferate. Cancer cell bioenergetics is mainly determined by a complex interplay of genetic, biochemical, microenvironmental and immunological factors. In general, glucose and fatty acids are the two major fuels for mitochondria. Since Otto Warburg formulated his theory on the importance of cancer metabolism, in 1924, we have learned a lot about the complexity of this process.
Many types of cancer cells can acquire metabolic plasticity by gaining a hybrid glycolysis/OxPhos phenotype. It is still largely unknown how cancer cells orchestrate the energy production, energy consumption, and transfer pathways to regulate their glycolytic and OxPhos activities and what components are involved in these processes. For example, inhibitors targeting glycolysis may also affect multiple other pathways during metabolic reprogramming, including OxPhos.
In addition to metabolic interactions, the genetic interplay, epithelial plasticity and covalent modifications (phosphorylation, acetylation, and glycosylation) may also play an important role in the mechanisms of cancer metabolic plasticity. The link between phosphotransfer performance and metabolic plasticity of cancer cells associated with the cell differentiation state should also be considered. Cancer stem cells (CSC) seem to be involved in the initiation of tumor metastasis and tumor relapse, and they show remarkable resistance to chemo- and radiotherapy. CSC exhibit unique metabolic flexibility, and in most cancer types may develop a typical “energetic” CSC phenotype.
This Research Topic will highlight the complexity of the molecular (genetic, biochemical) mechanisms that regulate the mitochondrial function at multiple levels leading to reprogramming of the cancer energy metabolism. We would like to integrate our current understanding of the different components of cancer metabolism involved in the metabolic plasticity in cancer cells. An improved understanding of the biochemical mechanisms and processes involved in tumor cells may open new approaches for metastatic cancer treatment. Possible subtopics of this article collection include:
1) The Krebs cycle and metabolic plasticity
2) Metabolic plasticity of cancer stem cells
3) Epigenetic modifications in cancer: metabolic reprogramming
4) Systems biology of cancer metabolic plasticity
5) Metabolic plasticity as the tool for adaptations of changes in the tumor microenvironment
6) Glycolysis and oxidative phosphorylation in cancer cells
7) Drug targeting of cancer energy metabolism
8) The role of mitochondrial energy transfer
9) Alterations in the mitochondrial outer membrane and apoptosis
We welcome Original Research and Review articles that focus on metabolic plasticity. Manuscripts with potential clinical applications may also be accepted but this approach will not be mandatory or exclusive.
Cancer cells use a variety of metabolic reprogramming strategies to survive and proliferate. Cancer cell bioenergetics is mainly determined by a complex interplay of genetic, biochemical, microenvironmental and immunological factors. In general, glucose and fatty acids are the two major fuels for mitochondria. Since Otto Warburg formulated his theory on the importance of cancer metabolism, in 1924, we have learned a lot about the complexity of this process.
Many types of cancer cells can acquire metabolic plasticity by gaining a hybrid glycolysis/OxPhos phenotype. It is still largely unknown how cancer cells orchestrate the energy production, energy consumption, and transfer pathways to regulate their glycolytic and OxPhos activities and what components are involved in these processes. For example, inhibitors targeting glycolysis may also affect multiple other pathways during metabolic reprogramming, including OxPhos.
In addition to metabolic interactions, the genetic interplay, epithelial plasticity and covalent modifications (phosphorylation, acetylation, and glycosylation) may also play an important role in the mechanisms of cancer metabolic plasticity. The link between phosphotransfer performance and metabolic plasticity of cancer cells associated with the cell differentiation state should also be considered. Cancer stem cells (CSC) seem to be involved in the initiation of tumor metastasis and tumor relapse, and they show remarkable resistance to chemo- and radiotherapy. CSC exhibit unique metabolic flexibility, and in most cancer types may develop a typical “energetic” CSC phenotype.
This Research Topic will highlight the complexity of the molecular (genetic, biochemical) mechanisms that regulate the mitochondrial function at multiple levels leading to reprogramming of the cancer energy metabolism. We would like to integrate our current understanding of the different components of cancer metabolism involved in the metabolic plasticity in cancer cells. An improved understanding of the biochemical mechanisms and processes involved in tumor cells may open new approaches for metastatic cancer treatment. Possible subtopics of this article collection include:
1) The Krebs cycle and metabolic plasticity
2) Metabolic plasticity of cancer stem cells
3) Epigenetic modifications in cancer: metabolic reprogramming
4) Systems biology of cancer metabolic plasticity
5) Metabolic plasticity as the tool for adaptations of changes in the tumor microenvironment
6) Glycolysis and oxidative phosphorylation in cancer cells
7) Drug targeting of cancer energy metabolism
8) The role of mitochondrial energy transfer
9) Alterations in the mitochondrial outer membrane and apoptosis
We welcome Original Research and Review articles that focus on metabolic plasticity. Manuscripts with potential clinical applications may also be accepted but this approach will not be mandatory or exclusive.
