About this Research Topic
Metabolism reprogramming is one of the hallmarks of cancer, which enables cancer cells to utilize nutrients in a low-nutrient environment and maintain bio-viability. Metabolic reprogramming, whether as a consequence or a driver of tumorigenesis, is closely linked to the progression of intrinsic biological phenotypes in cancer cells and is tightly regulated by oncogenes.
Numerous research showed that tumor metabolites are associated with malignant phenotypes including epithelial-mesenchymal transition (EMT), tumor proliferation, invasion, apoptosis, and ferroptosis inhibition. Meanwhile, the byproduct from cancer metabolism reprogramming reshapes the hostile tumor microenvironment, emerging studies revealed the metabolic crosstalk between tumor cells and T-cells, tumor-associated macrophages, cancer-associated fibroblasts, endothelium, adipocytes participate in tumor microenvironment remodel through different mechanisms.
The rapid advancement of RNA bulk sequencing, single-cell transcriptomics, and spatial transcriptomics technologies provides valuable insights into the tumor microenvironment, shedding light on the role of metabolism-associated tumor genes and the interactions between tumor cells and other cellular components in the context of metabolism. The peculiarities of tumor metabolism reprogramming endow potential chances for the development of therapeutic targets for tumor cells per se, and tumor-promoting microenvironment. One example is the application of adenosine-associated enzyme inhibitors in solid tumors to blockage the immune exhausting effect from adenosine-associated metabolites, which is undergoing phase II clinical trials.
Considering the emerging prospect of targeting tumor metabolism reprogramming and the mechanisms of metabolic crosstalk between tumor cells and tumor microenvironment remains largely ignorant, this Research Topic aims to converge the insights regarding the effect of tumor-derived metabolites in tumor microenvironment remodel and the underlying molecular mechanism through multi-omics data, single cell analysis, and spatial transcriptomics explore.
The goal is to unveil the fragile metabolic pathways in cancer compared with normal tissue and propose novel therapeutic strategies to interfere with the metabolic intersection between cancer cells/other cellular components and ultimately reverse the tumor-microenvironment remodel.
This Research Topic is looking for contributions regarding cancer metabolic reprogramming. We welcome Original Research, Brief Research Report, Methods, Mini Review, Opinion, Perspective, Review, Systematic Review articles which may address, but are not limited to, the following themes:
- The role of cancer cells-derived metabolites in inducing T cell exhaustion.
- Influence of cancer cells-derived metabolites on lymphangiogenesis/angiogenesis.
- The impact of cancer cells-derived metabolites on cancer-associated fibroblasts.
- Cancer cells-derived metabolites and macrophages polarization.
- Interactions between cancer-derived metabolites and various innate immune cells.
Numerous research showed that tumor metabolites are associated with malignant phenotypes including epithelial-mesenchymal transition (EMT), tumor proliferation, invasion, apoptosis, and ferroptosis inhibition. Meanwhile, the byproduct from cancer metabolism reprogramming reshapes the hostile tumor microenvironment, emerging studies revealed the metabolic crosstalk between tumor cells and T-cells, tumor-associated macrophages, cancer-associated fibroblasts, endothelium, adipocytes participate in tumor microenvironment remodel through different mechanisms.
The rapid advancement of RNA bulk sequencing, single-cell transcriptomics, and spatial transcriptomics technologies provides valuable insights into the tumor microenvironment, shedding light on the role of metabolism-associated tumor genes and the interactions between tumor cells and other cellular components in the context of metabolism. The peculiarities of tumor metabolism reprogramming endow potential chances for the development of therapeutic targets for tumor cells per se, and tumor-promoting microenvironment. One example is the application of adenosine-associated enzyme inhibitors in solid tumors to blockage the immune exhausting effect from adenosine-associated metabolites, which is undergoing phase II clinical trials.
Considering the emerging prospect of targeting tumor metabolism reprogramming and the mechanisms of metabolic crosstalk between tumor cells and tumor microenvironment remains largely ignorant, this Research Topic aims to converge the insights regarding the effect of tumor-derived metabolites in tumor microenvironment remodel and the underlying molecular mechanism through multi-omics data, single cell analysis, and spatial transcriptomics explore.
The goal is to unveil the fragile metabolic pathways in cancer compared with normal tissue and propose novel therapeutic strategies to interfere with the metabolic intersection between cancer cells/other cellular components and ultimately reverse the tumor-microenvironment remodel.
This Research Topic is looking for contributions regarding cancer metabolic reprogramming. We welcome Original Research, Brief Research Report, Methods, Mini Review, Opinion, Perspective, Review, Systematic Review articles which may address, but are not limited to, the following themes:
- The role of cancer cells-derived metabolites in inducing T cell exhaustion.
- Influence of cancer cells-derived metabolites on lymphangiogenesis/angiogenesis.
- The impact of cancer cells-derived metabolites on cancer-associated fibroblasts.
- Cancer cells-derived metabolites and macrophages polarization.
- Interactions between cancer-derived metabolites and various innate immune cells.
Keywords: Cancer metabolism, Tumor microenvironment, Tumor progression, Immunosurveillance, Therapy
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.
