Metastasis is a major contributor to cancer-associated deaths, and its investigation and treatment are of great interest to both researchers and clinicians. It entails intricate interactions between primary tumorigenic sites and potential metastatic sites. Following their development, primary tumors actively cooperate with the host’s stromal and immune cells to form the pre-metastatic niche (PMN). Despite numerous approaches to understanding the evolution of the PMN and potential ways to control it, a clear picture is still lacking.
The PMN is a key player in the development of metastasis as it offers an opportunity for circulating tumor cells (CTCs), detached from the primary tumor, to adapt and colonies secondary sites. As a result, CTCs develop into disseminated tumor cells, multiply and enable the emergence of subsequent metastasis. In support of the “seed and soil” theory, the PMN undergoes molecular and cellular changes to generate a favorable ecosystem (the fertile soil) in the preparation of the metastatic tumor cells (the seed). Some of these components have been identified in various preclinical tumor models and linked to different patterns of organ tropism and metastasis. The PMN results from combined systemic effects of secreted soluble factors and shaded extracellular vesicles released by the primary tumor cells, myeloid cells, and local stromal cells, all in a certain temporary sequence. The secretion of these factors (e.g. cytokines, chemokines, growth factors, extracellular matrix (ECM) remodeling, and metabolic reprogramming factors) and vesicles mediates the communication from local to distant sites and seems to be the main drivers that trigger changes in the host microenvironment, functional alteration of the resident cells, recruitment of bone marrow-derived cells and other types of immune cells.
This Research Topic aims to gain new insights on the molecular and cellular mechanisms that lead the PMN formation and functions in order to direct future research into the underlying mechanisms of metastasis for developing more effective cancer diagnostic and therapeutic strategies. We welcome Original Research Articles and Review Articles focused on, but not limited to:
- Cellular signaling pathways implicated in the PMN
- Cellular components of the PMN
- Extracellular vesicles that allow for efficient tumor cell colonization
- Vascular alterations that support PMN formation
- Hypoxia control of the PMN
- Inflammation and Immunosuppression and the development of PMN
- Metabolic reprogramming and its crucial role in PMN
- Remodelling the microenvironment of the PMN
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.
Metastasis is a major contributor to cancer-associated deaths, and its investigation and treatment are of great interest to both researchers and clinicians. It entails intricate interactions between primary tumorigenic sites and potential metastatic sites. Following their development, primary tumors actively cooperate with the host’s stromal and immune cells to form the pre-metastatic niche (PMN). Despite numerous approaches to understanding the evolution of the PMN and potential ways to control it, a clear picture is still lacking.
The PMN is a key player in the development of metastasis as it offers an opportunity for circulating tumor cells (CTCs), detached from the primary tumor, to adapt and colonies secondary sites. As a result, CTCs develop into disseminated tumor cells, multiply and enable the emergence of subsequent metastasis. In support of the “seed and soil” theory, the PMN undergoes molecular and cellular changes to generate a favorable ecosystem (the fertile soil) in the preparation of the metastatic tumor cells (the seed). Some of these components have been identified in various preclinical tumor models and linked to different patterns of organ tropism and metastasis. The PMN results from combined systemic effects of secreted soluble factors and shaded extracellular vesicles released by the primary tumor cells, myeloid cells, and local stromal cells, all in a certain temporary sequence. The secretion of these factors (e.g. cytokines, chemokines, growth factors, extracellular matrix (ECM) remodeling, and metabolic reprogramming factors) and vesicles mediates the communication from local to distant sites and seems to be the main drivers that trigger changes in the host microenvironment, functional alteration of the resident cells, recruitment of bone marrow-derived cells and other types of immune cells.
This Research Topic aims to gain new insights on the molecular and cellular mechanisms that lead the PMN formation and functions in order to direct future research into the underlying mechanisms of metastasis for developing more effective cancer diagnostic and therapeutic strategies. We welcome Original Research Articles and Review Articles focused on, but not limited to:
- Cellular signaling pathways implicated in the PMN
- Cellular components of the PMN
- Extracellular vesicles that allow for efficient tumor cell colonization
- Vascular alterations that support PMN formation
- Hypoxia control of the PMN
- Inflammation and Immunosuppression and the development of PMN
- Metabolic reprogramming and its crucial role in PMN
- Remodelling the microenvironment of the PMN
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.
