Metabolic alterations and immune evasion represent some of the hallmark capabilities of tumor cells developed during multistep metastatic progression. Cancer cells undergo significant metabolic reprogramming as they adapt to survive in environments with varying nutrient and energy availability as well as different oxygen concentrations, eventually forming distant metastasis. Many metabolic pathways, including aerobic glycolysis, amino acid, and lipid metabolism have been shown to support the metastatic process by modulating ATP production, tumor microenvironment pH, redox balance, generation of reactive oxygen species (ROS) and more. In addition, cancer cells utilize multiple mechanisms by which they evade destruction by the immune system. The loss of immune surveillance further facilitates tumor progression and many different inflammatory cells including myeloid-derived suppressor cells (MDSC), macrophages, Treg, dendritic cells, and effector CD4+ and CD8+ T lymphocytes have been shown to participate in cancer cell dissemination and metastatic outgrowth at the secondary tumor site.
The modulation of cancer cell metabolism and immune response may represent the key strategy to treat cancer by preventing tumor metastasis and recurrence. To target metastases effectively, it is important to understand the critical function of altered bioenergetics, metabolic flux, carbohydrate, lipid as well as amino acid metabolism, and oncoimmunological associated modulations such as cytokines and chemokines adopted by cancer cells during the metastatic process. Given recent evidence showing that immunotherapy (immune checkpoint pathway inhibitors, adoptive cell therapies and metabolic inhibitors such as GLUT inhibitor as well as OXPHOS inhibitor) provide promising approaches for the treatment of cancer, we speculate that anti-metastasis strategies using metabolic inhibitors, and immunotherapy could provide a comprehensive means to better control tumor progression.
This Research Topic will focus on the latest advances in cancer metabolism and oncoimmunology research in the context of cancer metastasis. We welcome Original Research as well as Review articles including, but not strictly limited to:
1) Metabolic reprogramming of cancer and stromal cells in cancer metastasis, including bioenergetics, metabolic flux, and carbohydrate, lipid, and amino acid metabolism.
2) Alterations in the inflammatory cells including MDSC, macrophages, Treg, dendritic cells, and effector CD4+ and CD8+ T lymphocytes, as well as mediators such as cytokines, chemokines and other reactive molecules in cancer metastasis, and potential applications in targeting cancer metastasis
3) The mechanism of metabolic reprogramming and immune evasion in cancer metastasis with epigenetic, transcriptional and post-translational regulation.
4) Metabolic reprogramming and immune-modulatory effects in drug-resistant metastatic cancer cells.
5) Metabolic abnormalities and immune evasion in cancer metastasis led by tumor-associated genes (oncogene activation or tumor suppressor gene deletion, or inactivation), micro-environmental factors, transcription factors, non-coding RNAs, the mutation/-modification/epigenetic regulation of regulatory proteins.
Metabolic alterations and immune evasion represent some of the hallmark capabilities of tumor cells developed during multistep metastatic progression. Cancer cells undergo significant metabolic reprogramming as they adapt to survive in environments with varying nutrient and energy availability as well as different oxygen concentrations, eventually forming distant metastasis. Many metabolic pathways, including aerobic glycolysis, amino acid, and lipid metabolism have been shown to support the metastatic process by modulating ATP production, tumor microenvironment pH, redox balance, generation of reactive oxygen species (ROS) and more. In addition, cancer cells utilize multiple mechanisms by which they evade destruction by the immune system. The loss of immune surveillance further facilitates tumor progression and many different inflammatory cells including myeloid-derived suppressor cells (MDSC), macrophages, Treg, dendritic cells, and effector CD4+ and CD8+ T lymphocytes have been shown to participate in cancer cell dissemination and metastatic outgrowth at the secondary tumor site.
The modulation of cancer cell metabolism and immune response may represent the key strategy to treat cancer by preventing tumor metastasis and recurrence. To target metastases effectively, it is important to understand the critical function of altered bioenergetics, metabolic flux, carbohydrate, lipid as well as amino acid metabolism, and oncoimmunological associated modulations such as cytokines and chemokines adopted by cancer cells during the metastatic process. Given recent evidence showing that immunotherapy (immune checkpoint pathway inhibitors, adoptive cell therapies and metabolic inhibitors such as GLUT inhibitor as well as OXPHOS inhibitor) provide promising approaches for the treatment of cancer, we speculate that anti-metastasis strategies using metabolic inhibitors, and immunotherapy could provide a comprehensive means to better control tumor progression.
This Research Topic will focus on the latest advances in cancer metabolism and oncoimmunology research in the context of cancer metastasis. We welcome Original Research as well as Review articles including, but not strictly limited to:
1) Metabolic reprogramming of cancer and stromal cells in cancer metastasis, including bioenergetics, metabolic flux, and carbohydrate, lipid, and amino acid metabolism.
2) Alterations in the inflammatory cells including MDSC, macrophages, Treg, dendritic cells, and effector CD4+ and CD8+ T lymphocytes, as well as mediators such as cytokines, chemokines and other reactive molecules in cancer metastasis, and potential applications in targeting cancer metastasis
3) The mechanism of metabolic reprogramming and immune evasion in cancer metastasis with epigenetic, transcriptional and post-translational regulation.
4) Metabolic reprogramming and immune-modulatory effects in drug-resistant metastatic cancer cells.
5) Metabolic abnormalities and immune evasion in cancer metastasis led by tumor-associated genes (oncogene activation or tumor suppressor gene deletion, or inactivation), micro-environmental factors, transcription factors, non-coding RNAs, the mutation/-modification/epigenetic regulation of regulatory proteins.
