About this Research Topic
Since Conrad Waddington introduced the term “epigenetics” in 1942, its definition has wildly changed and evolved in parallel to our knowledge of the phenomenon.
Today, epigenetics is considered the study of hereditable changes in gene activity and regulation, that are not associated with modifications in the underlying DNA sequence. Over the past 80 years, the field of epigenetics has revolutionized the life sciences, changing our concept of biological processes and encompassing the spectrum of research, from basic research to translational and clinical research.
At Frontiers in Oncology, we would like to celebrate this incredible journey and the impact that epigenetic studies have had in the oncology field by introducing this special series. In this series, we would like to explore the recent advances in epigenetic studies in the most significant fields of oncological research with the greater aim of benefiting patients and cancer prevention in our communities.
Epigenetic Insights into Cancer Metabolism
Metabolism is altered in cancer cells as they need to meet the energetic demands of continuous proliferation. The most common metabolic alterations observed in tumors include increased glutaminolysis and aerobic glycolysis, deregulation of lipid metabolism, and increased generation of reactive oxygen species (ROS). Cancer metabolic reprogramming is considered one of the hallmarks of cancer, as it promotes carcinogenesis and tumor progression enabling rapid proliferation, survival, metastasis, and resistance to therapies.
Cancer metabolic reprogramming is tightly connected to cancer-associated epigenetic changes.
One of the key enzymes of glucose metabolism pathways, Hexokinase 2, has been reported to be upregulated in glioblastoma and liver cancer patients due to the hypomethylation found at the gene promoter region. Conversely, the hypermethylation of fructose 1,6-biphosphatase promoter silence the enzyme expression and promote higher glycolytic rates in different tumors, such as breast cancer, gastric cancer, and lung cancer.
The deregulation of key metabolic enzymes due to aberrant epigenetic events can be coupled with wide-metabolic effects on the epigenetic landscape of tumor cells. Abnormal activities of glycolytic enzymes affect the abundance of acetyl-coenzyme A (acetyl-CoA) which acts as substrate for histone acetyltransferases. Similarly, Altered S-adenosyl methionine (SAM) metabolism in cancer results in higher intracellular levels of SAM, a universal methyl donor for methylation reaction, including DNA and histone methylations.
This interplay between metabolism and epigenetic changes is recognized to play a crucial role in cancer development and progression, but we have just scratched the surface of the multiple connections between metabolic reprogramming and epigenetic regulations in cancer.
This Research Topic aims to explore, but is not limited to the following:
- non-coding RNAs as modulators of metabolic pathways in cancer
- metabolite-driven epigenetic regulation of metabolic genes and/or oncogenic cascades
- the role of the tumor microenvironment in the metabolism-epigenetic crosstalk
- newly identified oncometabolites
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.
See below for other collections in the Epigenetic Insights series:
- Epigenetic Insights into Carcinogenesis
- Epigenetic Insights into Diagnostic and Therapeutic Applications
- Epigenetic Insights into Diet and Nutrition in Cancer
Today, epigenetics is considered the study of hereditable changes in gene activity and regulation, that are not associated with modifications in the underlying DNA sequence. Over the past 80 years, the field of epigenetics has revolutionized the life sciences, changing our concept of biological processes and encompassing the spectrum of research, from basic research to translational and clinical research.
At Frontiers in Oncology, we would like to celebrate this incredible journey and the impact that epigenetic studies have had in the oncology field by introducing this special series. In this series, we would like to explore the recent advances in epigenetic studies in the most significant fields of oncological research with the greater aim of benefiting patients and cancer prevention in our communities.
Epigenetic Insights into Cancer Metabolism
Metabolism is altered in cancer cells as they need to meet the energetic demands of continuous proliferation. The most common metabolic alterations observed in tumors include increased glutaminolysis and aerobic glycolysis, deregulation of lipid metabolism, and increased generation of reactive oxygen species (ROS). Cancer metabolic reprogramming is considered one of the hallmarks of cancer, as it promotes carcinogenesis and tumor progression enabling rapid proliferation, survival, metastasis, and resistance to therapies.
Cancer metabolic reprogramming is tightly connected to cancer-associated epigenetic changes.
One of the key enzymes of glucose metabolism pathways, Hexokinase 2, has been reported to be upregulated in glioblastoma and liver cancer patients due to the hypomethylation found at the gene promoter region. Conversely, the hypermethylation of fructose 1,6-biphosphatase promoter silence the enzyme expression and promote higher glycolytic rates in different tumors, such as breast cancer, gastric cancer, and lung cancer.
The deregulation of key metabolic enzymes due to aberrant epigenetic events can be coupled with wide-metabolic effects on the epigenetic landscape of tumor cells. Abnormal activities of glycolytic enzymes affect the abundance of acetyl-coenzyme A (acetyl-CoA) which acts as substrate for histone acetyltransferases. Similarly, Altered S-adenosyl methionine (SAM) metabolism in cancer results in higher intracellular levels of SAM, a universal methyl donor for methylation reaction, including DNA and histone methylations.
This interplay between metabolism and epigenetic changes is recognized to play a crucial role in cancer development and progression, but we have just scratched the surface of the multiple connections between metabolic reprogramming and epigenetic regulations in cancer.
This Research Topic aims to explore, but is not limited to the following:
- non-coding RNAs as modulators of metabolic pathways in cancer
- metabolite-driven epigenetic regulation of metabolic genes and/or oncogenic cascades
- the role of the tumor microenvironment in the metabolism-epigenetic crosstalk
- newly identified oncometabolites
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.
See below for other collections in the Epigenetic Insights series:
- Epigenetic Insights into Carcinogenesis
- Epigenetic Insights into Diagnostic and Therapeutic Applications
- Epigenetic Insights into Diet and Nutrition in Cancer
Keywords: Epigenetic, cancer metabolic reprograming, oncometabolites, ncRNAs, tumor microenvironment, metabolite-driven epigenetic regulation, metabolism-epigenetic crosstalk
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.
