Dysregulation of epigenetics has been identified as a key feature of various cancers. Scientists have been exploring new drugs that target the potential epigenetic writers, readers, and erasers. To date, the U.S. Food and Drug Administration (FDA) has approved several cancer drugs targeting epigenomes. Due to the unsatisfactory efficacy of monotherapy with epigenome-targeted therapies in most solid tumors, various combination strategies have been explored. For example, the epigenetic drugs, including tazemetostat, are often used in clinical trials in combination with other drugs such as romidepsin (HDAC inhibitor) and etoposide (a chemotherapy regimen) to treat patients with relapsed or refractory peripheral T-cell lymphoma.
Meanwhile, epigenetic alteration is interplayed with metabolic reprogramming, a hallmark in cancer . During tumorigenesis or progression, cancer cells take up high amounts of glucose even in aerobic environments and produce lactic acid by glycolysis, a phenomenon known as the "Warburg effect". In addition to glucose, glutamine may also serve as an energy source for tumor cell biosynthesis and act as a nitrogen donor. Furthermore, lipid metabolism of cancer cells is characterized by the storage of excess lipids and cholesterol in lipid droplets (LDs). High levels of LDs and cholesterol esters in tumors are now considered indicators of cancer aggressiveness. Based on these discoveries, the strategy to regulate metabolism has attracted increasing attention in the field of anticancer drugs.
There is growing evidence that epigenetic and metabolic changes in cancer cells are closely intertwined. A combination of interventions in epigenetic regulation and metabolic activities of tumor cells could help to achieve better therapeutic effects. For example, the scientists identified that metformin-stimulated AMPK signaling converges at FOXO3 to stimulate SETD2 expression, which is the methyl-transferase of H3K36. In addition, the interplay between SETD2-EZH2 axis can further integrate metabolic and epigenetic signaling to restrict PCa metastasis. A number of clinical trials are under way for hematologic malignancies and solid tumors.
In this Research Topic, we call for submissions that address epi-drugs in cancer therapy and mono- or combination metabolic drugs, as well as basic research on epigenetic and metabolic reprogramming in cancer. Epi-drugs include all agents targeting DNA and/or histone modifications, as well as potential ncRNA/RNA modification targets.
The aim of this Research Topic is to highlight the work in the field of epi-drugs and metabolic approaches in cancer therapy, with a particular focus on finding a better strategy for the use of epi-drugs as single or combination drugs. What are the effects of these epi-drugs on cancer metabolism and how can these changes in metabolic patterns be exploited to achieve better efficacy?
The following sub-topics are included in the Research Topic, but are not limited to:
● Histone modification targeted anti-cancer drugs.
● DNA modification targeted anti-cancer drugs.
● RNA modification targeted anti-cancer drugs.
● ncRNA targeted anti-cancer drugs.
● Metabolic regulatory anti-cancer drugs.
Article types include Brief Research Report, Case Report, Clinical Trial, Data Report, Editorial, Erratum, Hypothesis and Theory, Methods, Mini Review, Opinion, Original Research, Perspective, Review, Systematic Review and Technology and Code.
Dysregulation of epigenetics has been identified as a key feature of various cancers. Scientists have been exploring new drugs that target the potential epigenetic writers, readers, and erasers. To date, the U.S. Food and Drug Administration (FDA) has approved several cancer drugs targeting epigenomes. Due to the unsatisfactory efficacy of monotherapy with epigenome-targeted therapies in most solid tumors, various combination strategies have been explored. For example, the epigenetic drugs, including tazemetostat, are often used in clinical trials in combination with other drugs such as romidepsin (HDAC inhibitor) and etoposide (a chemotherapy regimen) to treat patients with relapsed or refractory peripheral T-cell lymphoma.
Meanwhile, epigenetic alteration is interplayed with metabolic reprogramming, a hallmark in cancer . During tumorigenesis or progression, cancer cells take up high amounts of glucose even in aerobic environments and produce lactic acid by glycolysis, a phenomenon known as the "Warburg effect". In addition to glucose, glutamine may also serve as an energy source for tumor cell biosynthesis and act as a nitrogen donor. Furthermore, lipid metabolism of cancer cells is characterized by the storage of excess lipids and cholesterol in lipid droplets (LDs). High levels of LDs and cholesterol esters in tumors are now considered indicators of cancer aggressiveness. Based on these discoveries, the strategy to regulate metabolism has attracted increasing attention in the field of anticancer drugs.
There is growing evidence that epigenetic and metabolic changes in cancer cells are closely intertwined. A combination of interventions in epigenetic regulation and metabolic activities of tumor cells could help to achieve better therapeutic effects. For example, the scientists identified that metformin-stimulated AMPK signaling converges at FOXO3 to stimulate SETD2 expression, which is the methyl-transferase of H3K36. In addition, the interplay between SETD2-EZH2 axis can further integrate metabolic and epigenetic signaling to restrict PCa metastasis. A number of clinical trials are under way for hematologic malignancies and solid tumors.
In this Research Topic, we call for submissions that address epi-drugs in cancer therapy and mono- or combination metabolic drugs, as well as basic research on epigenetic and metabolic reprogramming in cancer. Epi-drugs include all agents targeting DNA and/or histone modifications, as well as potential ncRNA/RNA modification targets.
The aim of this Research Topic is to highlight the work in the field of epi-drugs and metabolic approaches in cancer therapy, with a particular focus on finding a better strategy for the use of epi-drugs as single or combination drugs. What are the effects of these epi-drugs on cancer metabolism and how can these changes in metabolic patterns be exploited to achieve better efficacy?
The following sub-topics are included in the Research Topic, but are not limited to:
● Histone modification targeted anti-cancer drugs.
● DNA modification targeted anti-cancer drugs.
● RNA modification targeted anti-cancer drugs.
● ncRNA targeted anti-cancer drugs.
● Metabolic regulatory anti-cancer drugs.
Article types include Brief Research Report, Case Report, Clinical Trial, Data Report, Editorial, Erratum, Hypothesis and Theory, Methods, Mini Review, Opinion, Original Research, Perspective, Review, Systematic Review and Technology and Code.