Epigenomics refers to the study of genome-wide changes in epigenetic mechanisms, which includes histone modifications, DNA methylation, and non-coding RNAs expression. Dysregulation of epigenetic mechanisms such as chromatin remodeling and post-translational DNA/histone modifications may result in altered gene expression profiles facilitating tumor development and progression. Metabolic alterations play an important role in the regulation of gene expression and have been recognized as a crucial hallmark of cancer due to gene mutations in specific metabolic enzymes or dietary/environmental factors. New intricate crosstalk between epigenetic and metabolic reprogramming has been unraveled in cancer over the past decade, thus making epigenetics and metabolism highly interplayed in a bidirectional manner. Metabolites that are generated during metabolic pathways serve as cofactors or substrates for the enzymatic reactions that catalyze epigenetic modifications and transcriptional regulation. Many studies have shown that the epigenome is sensitive to cellular metabolism. Although it has made new developments in these fields, some of the aspects pertaining to metabolic reprogramming and epigenetic modifications in cancers remain poorly understood. To elucidate crosstalk between epigenetic and metabolic reprogramming is imperative for deciphering the potential targets that can be exploited for the development of anti-cancer therapies.
The aims of this Research Topic are:
(1) To delineate the role of epigenetic/epigenomic and metabolic dysregulations and their crosstalk in tumorigenesis.
(2) To uncover the role of epigenetic mechanisms, including histone modifications, DNA methylation, non-coding RNAs, and mRNA modifications, such as N6-methyladenosine (m6A) in tumorigenesis.
We welcome submissions of Original Research, Reviews, Mini-Reviews, and Systematic Reviews that explore a wide range of topics include, but are not limited to, the following:
• How dysregulation of epigenetic mechanisms including chromatin remodeling and post-translational DNA/histone modifications may lead to tumor formation.
• How metabolism and epigenetics are highly interplayed, and their aberrant crosstalk can contribute to tumorigenesis.
• The role of oncogene-driven metabolic plasticity in tumorigenesis.
• How cancer cells acquire aggressive traits and shape tumor microenvironment through the crosstalk of epigenetics-metabolism.
• How oncogene or the DNA/histone-modifying enzymes affect metabolic reprogramming in cancer.
• How oncometabolite acting as the epigenetic modification enzyme’s regulators affect the epigenome during tumorigenesis.
• Epigenetics/epigenomics of phytochemicals in cancer prevention and treatments.
• Epigenetics/epigenomics of phytochemicals in cancer prevention and treatments.
Epigenomics refers to the study of genome-wide changes in epigenetic mechanisms, which includes histone modifications, DNA methylation, and non-coding RNAs expression. Dysregulation of epigenetic mechanisms such as chromatin remodeling and post-translational DNA/histone modifications may result in altered gene expression profiles facilitating tumor development and progression. Metabolic alterations play an important role in the regulation of gene expression and have been recognized as a crucial hallmark of cancer due to gene mutations in specific metabolic enzymes or dietary/environmental factors. New intricate crosstalk between epigenetic and metabolic reprogramming has been unraveled in cancer over the past decade, thus making epigenetics and metabolism highly interplayed in a bidirectional manner. Metabolites that are generated during metabolic pathways serve as cofactors or substrates for the enzymatic reactions that catalyze epigenetic modifications and transcriptional regulation. Many studies have shown that the epigenome is sensitive to cellular metabolism. Although it has made new developments in these fields, some of the aspects pertaining to metabolic reprogramming and epigenetic modifications in cancers remain poorly understood. To elucidate crosstalk between epigenetic and metabolic reprogramming is imperative for deciphering the potential targets that can be exploited for the development of anti-cancer therapies.
The aims of this Research Topic are:
(1) To delineate the role of epigenetic/epigenomic and metabolic dysregulations and their crosstalk in tumorigenesis.
(2) To uncover the role of epigenetic mechanisms, including histone modifications, DNA methylation, non-coding RNAs, and mRNA modifications, such as N6-methyladenosine (m6A) in tumorigenesis.
We welcome submissions of Original Research, Reviews, Mini-Reviews, and Systematic Reviews that explore a wide range of topics include, but are not limited to, the following:
• How dysregulation of epigenetic mechanisms including chromatin remodeling and post-translational DNA/histone modifications may lead to tumor formation.
• How metabolism and epigenetics are highly interplayed, and their aberrant crosstalk can contribute to tumorigenesis.
• The role of oncogene-driven metabolic plasticity in tumorigenesis.
• How cancer cells acquire aggressive traits and shape tumor microenvironment through the crosstalk of epigenetics-metabolism.
• How oncogene or the DNA/histone-modifying enzymes affect metabolic reprogramming in cancer.
• How oncometabolite acting as the epigenetic modification enzyme’s regulators affect the epigenome during tumorigenesis.
• Epigenetics/epigenomics of phytochemicals in cancer prevention and treatments.
• Epigenetics/epigenomics of phytochemicals in cancer prevention and treatments.
