In the early 20th century, Warburg showed that tumors produce more lactic acid than non-tumor cells. Warburg’s findings led to enhanced glycolysis being in the spotlight of cancer metabolism for several decades. However, in the last 20-30 years, accumulated experimental evidence demonstrated the role of functional mitochondria as another major metabolic contributor to tumor progression. The combination of older and more recent perspectives, moved the field into a consensus that enhanced glycolysis and oxidative metabolism coexist, and are interdependent. Moreover, cell proliferation in heterogeneous and metabolically flexible tumors is influenced both by mitochondrial metabolism and glycolysis. Thus, the study of mitochondrial function, serves the purpose of promoting a more comprehensive understanding of cancer metabolism that eventually, may lead to the development of novel pharmacological interventions to inhibit tumor growth.
A direct link between the magnitude of glycolysis and tumor malignancy, has been common ground in cancer biology. However, this concept is currently challenged by the identification of predominantly glycolytic or oxidative subsets in highly malignant tumors, and by accumulated evidence both in situ and in vivo. Thus, the metabolism of highly proliferating tumors does not depend exclusively on a high rate of glycolysis, as originally thought. The metabolic heterogeneity of tumors, an emerging field of research, proves that the metabolism of cancer cells is very dynamic. The adaptability of cancer cells to the utilization of mitochondrial metabolism or glycolysis as the main source of energy and metabolic intermediaries, is critical to better understand tumor biology and resistance to chemotherapy. The goal of this topic will be to request contributions from investigators from basic biology to translational approaches to mitochondrial metabolism in cancer.
This Research Topic intends to create a common space for investigators working on mitochondrial research in cancer to contribute advances, comprehensive revisions, or theoretical considerations relevant to the field. Contributions are expected to focus in:
1. Any aspect of mitochondrial biology to explain the relationship between mitochondrial metabolism and cell proliferation
2. Translational approaches, including drug-discovery or the utilization of current available drugs, to inhibit tumor growth through modification of mitochondrial metabolism.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
In the early 20th century, Warburg showed that tumors produce more lactic acid than non-tumor cells. Warburg’s findings led to enhanced glycolysis being in the spotlight of cancer metabolism for several decades. However, in the last 20-30 years, accumulated experimental evidence demonstrated the role of functional mitochondria as another major metabolic contributor to tumor progression. The combination of older and more recent perspectives, moved the field into a consensus that enhanced glycolysis and oxidative metabolism coexist, and are interdependent. Moreover, cell proliferation in heterogeneous and metabolically flexible tumors is influenced both by mitochondrial metabolism and glycolysis. Thus, the study of mitochondrial function, serves the purpose of promoting a more comprehensive understanding of cancer metabolism that eventually, may lead to the development of novel pharmacological interventions to inhibit tumor growth.
A direct link between the magnitude of glycolysis and tumor malignancy, has been common ground in cancer biology. However, this concept is currently challenged by the identification of predominantly glycolytic or oxidative subsets in highly malignant tumors, and by accumulated evidence both in situ and in vivo. Thus, the metabolism of highly proliferating tumors does not depend exclusively on a high rate of glycolysis, as originally thought. The metabolic heterogeneity of tumors, an emerging field of research, proves that the metabolism of cancer cells is very dynamic. The adaptability of cancer cells to the utilization of mitochondrial metabolism or glycolysis as the main source of energy and metabolic intermediaries, is critical to better understand tumor biology and resistance to chemotherapy. The goal of this topic will be to request contributions from investigators from basic biology to translational approaches to mitochondrial metabolism in cancer.
This Research Topic intends to create a common space for investigators working on mitochondrial research in cancer to contribute advances, comprehensive revisions, or theoretical considerations relevant to the field. Contributions are expected to focus in:
1. Any aspect of mitochondrial biology to explain the relationship between mitochondrial metabolism and cell proliferation
2. Translational approaches, including drug-discovery or the utilization of current available drugs, to inhibit tumor growth through modification of mitochondrial metabolism.
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.