Tumor cells are characterized by resistance to cell death, and they generally need more nutrients to survive and grow than normal cells. Glycolysis and glutaminolysis pathways are upregulated during tumorigenesis to enhance the tricarboxylic acid (TCA) cycle to provide multiple metabolites such as nucleotides, lipids, and amino acids. The generation of reactive oxygen species (ROS) through oxidative metabolism is also tightly regulated to reach redox balance during tumor initiation and progression. In addition to tumor cells in the tumor microenvironment (TME), metabolic crosstalk of various cell types including endothelial cells, fibroblasts, and immune cells can regulate tumor progression. Tumor metabolites have recently been recognized as signaling molecules that promote tumor growth by controlling gene expression beyond their biosynthetic roles. Besides, the metabolic adaptation of cancer cells could breakthrough metabolic constraints to metastasize and colonize distal sites. Based on the given important roles of tumor metabolism in tumorigenesis and progression, it is of great value to further investigate the underlying mechanism and provide research basis to develop metabolism therapies via promoting cancer death through enhancement of ferroptosis, apoptosis, pyroptosis, and senescence.
We aim to focus on the mechanisms that antagonize tumor resistance to cell death signals by metabolism reprogramming via promoting cell ferroptosis, apoptosis, pyroptosis, and senescence. We wish to explore many aspects involved in cancer metabolism and crosstalk of various cells within the TME and build on our understanding of how they all work together in tumorigenesis and progression, while simultaneously looking to the future of where this might take us. We propose to identify specific metabolic vulnerabilities in specific cancers, targeting to synergize with radiation, chemotherapy, or immunotherapy to induce selective cancer cell death.
This Research Topic welcomes high-quality Original Research, Review, and Perspective articles focusing on the relationship between metabolism reprogramming and cancer cell fate such as ferroptosis, apoptosis, pyroptosis, and senescence.
• Explorations of metabolic and signaling pathways involved in cancer cell growth: regulating the production of nucleic acids, lipids, amino acids, and ATP to sustain tumor cell survival as the main energy.
• Studies of the role of metabolism reprogramming, such as glycolysis, glutaminolysis, and lipid synthesis, in determining cancer cell fate, especially ferroptosis, apoptosis, pyroptosis, and senescence.
• Discoveries of new oncometabolites as signaling molecules that promote tumor growth by controlling gene expression.
• Identification of specific metabolic vulnerabilities within specific cancers, targeting of which would synergize with radiation, chemotherapy, or immunotherapy to induce selective cancer cell death.
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.
Tumor cells are characterized by resistance to cell death, and they generally need more nutrients to survive and grow than normal cells. Glycolysis and glutaminolysis pathways are upregulated during tumorigenesis to enhance the tricarboxylic acid (TCA) cycle to provide multiple metabolites such as nucleotides, lipids, and amino acids. The generation of reactive oxygen species (ROS) through oxidative metabolism is also tightly regulated to reach redox balance during tumor initiation and progression. In addition to tumor cells in the tumor microenvironment (TME), metabolic crosstalk of various cell types including endothelial cells, fibroblasts, and immune cells can regulate tumor progression. Tumor metabolites have recently been recognized as signaling molecules that promote tumor growth by controlling gene expression beyond their biosynthetic roles. Besides, the metabolic adaptation of cancer cells could breakthrough metabolic constraints to metastasize and colonize distal sites. Based on the given important roles of tumor metabolism in tumorigenesis and progression, it is of great value to further investigate the underlying mechanism and provide research basis to develop metabolism therapies via promoting cancer death through enhancement of ferroptosis, apoptosis, pyroptosis, and senescence.
We aim to focus on the mechanisms that antagonize tumor resistance to cell death signals by metabolism reprogramming via promoting cell ferroptosis, apoptosis, pyroptosis, and senescence. We wish to explore many aspects involved in cancer metabolism and crosstalk of various cells within the TME and build on our understanding of how they all work together in tumorigenesis and progression, while simultaneously looking to the future of where this might take us. We propose to identify specific metabolic vulnerabilities in specific cancers, targeting to synergize with radiation, chemotherapy, or immunotherapy to induce selective cancer cell death.
This Research Topic welcomes high-quality Original Research, Review, and Perspective articles focusing on the relationship between metabolism reprogramming and cancer cell fate such as ferroptosis, apoptosis, pyroptosis, and senescence.
• Explorations of metabolic and signaling pathways involved in cancer cell growth: regulating the production of nucleic acids, lipids, amino acids, and ATP to sustain tumor cell survival as the main energy.
• Studies of the role of metabolism reprogramming, such as glycolysis, glutaminolysis, and lipid synthesis, in determining cancer cell fate, especially ferroptosis, apoptosis, pyroptosis, and senescence.
• Discoveries of new oncometabolites as signaling molecules that promote tumor growth by controlling gene expression.
• Identification of specific metabolic vulnerabilities within specific cancers, targeting of which would synergize with radiation, chemotherapy, or immunotherapy to induce selective cancer cell death.
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.
