In the last years, it has become evident that the tumor microenvironment composed by resident and infiltrating host cells is modulated by the multi-directional release and uptake of extracellular vesicles (EVs) from both tumor, stroma, and immune cells, ultimately stimulating tumor progression. The EV cargo of nucleic acids, proteins, and lipids has a role in the modulation of cancer stem cells phenotype associated with primary tumor maintenance, resistance to therapy, and dissemination to distant sites. In addition to their endogenous roles, EVs are currently being evaluated as delivery tools of various biomolecules (e.g., nucleic acids, lipids, proteins, and small molecule therapeutics) at both short and long distances. Thanks to their high stability in blood circulation, circulating EVs and their cargos could also be potential biomarkers for diagnosis and therapeutic response in cancer.
Cancer progression is a multistep process involving the growth, invasion, and dissemination of primary tumor cells to distant organs. The release of EVs by both tumor, immune, and stroma cells in the primary tumors has been linked to the all steps of tumor invasion and metastasis. The aim of this Research topic is to unveil how EVs participate to the mechanisms of primary tumor's escape and seeding of distant organs for metastasis establishment. Tumor or stroma EVs may lead to the acquisition of cancer stem cell phenotype endowing cells with self-renewal potential, tumorigenic and disseminating ability. Moreover, reprogramming of immune and stroma cells at distant sites by tumor-derived EVs leads to the establishment of the pre-metastatic niche (PMN) at the distant sites. Dissecting the EV-mediated mechanisms that induce CSC aggressive phenotype can help in understating how primary tumor cells acquire ability to intravasate, release into the blood stream as circulating tumor cells and disseminate to the PMN. Identification of potential inhibitors of EV-CSC and EV-PMN cross-talk can therefore prevent the acquisition of aggressive phenotype and metastatic potential of tumor cells.
We welcome Original Research, Review, Mini Review and Perspective articles on themes including, but not limited to:
- Role of extracellular vesicles in modulating the cross-talk of resident and host cells within the tumor microenvironment
- Role of extracellular vesicles in modulating cancer stem cell phenotype
- Role of extracellular vesicles in dictating primary tumor cells invasion and release of circulating tumor cells
- Role of extracellular vesicles in the formation of the pre-metastatic niche
- Role of extracellular vesicles in fostering metastasis formation
- Investigation of cargos of cancer-related extracellular vesicles as potential diagnostic and prognostic biomarkers
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
In the last years, it has become evident that the tumor microenvironment composed by resident and infiltrating host cells is modulated by the multi-directional release and uptake of extracellular vesicles (EVs) from both tumor, stroma, and immune cells, ultimately stimulating tumor progression. The EV cargo of nucleic acids, proteins, and lipids has a role in the modulation of cancer stem cells phenotype associated with primary tumor maintenance, resistance to therapy, and dissemination to distant sites. In addition to their endogenous roles, EVs are currently being evaluated as delivery tools of various biomolecules (e.g., nucleic acids, lipids, proteins, and small molecule therapeutics) at both short and long distances. Thanks to their high stability in blood circulation, circulating EVs and their cargos could also be potential biomarkers for diagnosis and therapeutic response in cancer.
Cancer progression is a multistep process involving the growth, invasion, and dissemination of primary tumor cells to distant organs. The release of EVs by both tumor, immune, and stroma cells in the primary tumors has been linked to the all steps of tumor invasion and metastasis. The aim of this Research topic is to unveil how EVs participate to the mechanisms of primary tumor's escape and seeding of distant organs for metastasis establishment. Tumor or stroma EVs may lead to the acquisition of cancer stem cell phenotype endowing cells with self-renewal potential, tumorigenic and disseminating ability. Moreover, reprogramming of immune and stroma cells at distant sites by tumor-derived EVs leads to the establishment of the pre-metastatic niche (PMN) at the distant sites. Dissecting the EV-mediated mechanisms that induce CSC aggressive phenotype can help in understating how primary tumor cells acquire ability to intravasate, release into the blood stream as circulating tumor cells and disseminate to the PMN. Identification of potential inhibitors of EV-CSC and EV-PMN cross-talk can therefore prevent the acquisition of aggressive phenotype and metastatic potential of tumor cells.
We welcome Original Research, Review, Mini Review and Perspective articles on themes including, but not limited to:
- Role of extracellular vesicles in modulating the cross-talk of resident and host cells within the tumor microenvironment
- Role of extracellular vesicles in modulating cancer stem cell phenotype
- Role of extracellular vesicles in dictating primary tumor cells invasion and release of circulating tumor cells
- Role of extracellular vesicles in the formation of the pre-metastatic niche
- Role of extracellular vesicles in fostering metastasis formation
- Investigation of cargos of cancer-related extracellular vesicles as potential diagnostic and prognostic biomarkers
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this topic.
