Cancer is a very complex disease where both genetic and environmental factors deeply affect tumor development, response to therapies, and metastatic spreading. Despite significant advances in the development of effective cancer treatments, resistance to anticancer therapies represents a critical hurdle for a cure. Conventional therapies such as chemotherapy and radiotherapy, as well as target therapy and immunotherapy not only induce a strong selective pressure on cancer cells but also profoundly alters the other cellular and acellular components of the tumor microenvironment (TME).
Changes in TME ecosystem contributes to the insurgence of resistant clones as result from both pre-existing and intrinsic factors as well as treatment-induced alterations. Indeed, the different treatments affect several pathways associated with cellular fate, including metabolism, also promoting the release of inflammatory and damage-associated molecules. Response to therapies strictly depends on metabolic state of the cells but cancer cells can also reprogram their metabolism as a possible adaptive resistance strategy. Remodeling of metabolic networks after treatment refers to several pathways, from glycolysis and oxidative phosphorylation to lipid and amino acid homeostasis.
In addition, it has been reported that metabolic reprogramming induces a less differentiated cellular state in cancer cells often associated with tumor recurrence. Nucleotides and nucleosides are present at high levels in cancer extracellular milieu after treatment, representing main drivers in metabolic reprogramming through the activation of their respective purinergic P1 and P2 receptors. Depending on the panel of P2 and P1 receptors expressed on the tumor and infiltrating inflammatory and stromal cells, and by the level of expression of nucleotide-hydrolyzing enzymes (CD39 and CD73) many different cell processes can be activated including cell death or proliferation, impacting on metabolic state of the different cellular components of the TME. In such a complex scenario, where several pathways interconnect to each other, dissecting the intricate molecular metabolic networks activated is essential to build new potential effective clinical interventions.
This Research Topic aims to discuss the emerging findings on metabolism reprogramming in association with purinergic signaling in the context of tumorigenesis, resistance to therapies and metastatic dissemination. We welcome Original Research Articles, Review Articles and Perspective Articles.
Topic includes, but are not limited to:
- Role of purinergic signaling in association to therapy-induced alteration in metabolism
- Nucleosides and nucleotides in TME after different anti-cancer treatments
- Metabolic reprogramming and cancer stem cells
- Purinergic receptors and metabolism in cancer
- Metabolic reprogramming of tumor-infiltrating immune cells by purinergic signaling
- Anti-Purinergic therapies in cancer
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.
Cancer is a very complex disease where both genetic and environmental factors deeply affect tumor development, response to therapies, and metastatic spreading. Despite significant advances in the development of effective cancer treatments, resistance to anticancer therapies represents a critical hurdle for a cure. Conventional therapies such as chemotherapy and radiotherapy, as well as target therapy and immunotherapy not only induce a strong selective pressure on cancer cells but also profoundly alters the other cellular and acellular components of the tumor microenvironment (TME).
Changes in TME ecosystem contributes to the insurgence of resistant clones as result from both pre-existing and intrinsic factors as well as treatment-induced alterations. Indeed, the different treatments affect several pathways associated with cellular fate, including metabolism, also promoting the release of inflammatory and damage-associated molecules. Response to therapies strictly depends on metabolic state of the cells but cancer cells can also reprogram their metabolism as a possible adaptive resistance strategy. Remodeling of metabolic networks after treatment refers to several pathways, from glycolysis and oxidative phosphorylation to lipid and amino acid homeostasis.
In addition, it has been reported that metabolic reprogramming induces a less differentiated cellular state in cancer cells often associated with tumor recurrence. Nucleotides and nucleosides are present at high levels in cancer extracellular milieu after treatment, representing main drivers in metabolic reprogramming through the activation of their respective purinergic P1 and P2 receptors. Depending on the panel of P2 and P1 receptors expressed on the tumor and infiltrating inflammatory and stromal cells, and by the level of expression of nucleotide-hydrolyzing enzymes (CD39 and CD73) many different cell processes can be activated including cell death or proliferation, impacting on metabolic state of the different cellular components of the TME. In such a complex scenario, where several pathways interconnect to each other, dissecting the intricate molecular metabolic networks activated is essential to build new potential effective clinical interventions.
This Research Topic aims to discuss the emerging findings on metabolism reprogramming in association with purinergic signaling in the context of tumorigenesis, resistance to therapies and metastatic dissemination. We welcome Original Research Articles, Review Articles and Perspective Articles.
Topic includes, but are not limited to:
- Role of purinergic signaling in association to therapy-induced alteration in metabolism
- Nucleosides and nucleotides in TME after different anti-cancer treatments
- Metabolic reprogramming and cancer stem cells
- Purinergic receptors and metabolism in cancer
- Metabolic reprogramming of tumor-infiltrating immune cells by purinergic signaling
- Anti-Purinergic therapies in cancer
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.
