Extracellular vesicles (EVs) secreted by tumor cells play a critical role in intercellular communication, contributing to both primary tumor growth and metastatic progression. These EVs, including exosomes, microvesicles, and oncosomes, contain bioactive molecules such as nucleic acids, proteins, and lipids that can alter the function of recipient cells. They promote angiogenesis, coagulation, immune modulation, and tissue remodeling, supporting tumor progression and metastasis. Clinically, EVs may serve as biomarkers and therapeutic targets for cancer progression, particularly for predicting and preventing future metastatic development. EVs are involved in various physiological processes, including coagulation, immune regulation, and development. They facilitate bidirectional communication between the embryo and uterine endometrium, contributing to successful implantation. EVs also play a role in pregnancy by promoting an immune-tolerant microenvironment. In cancer, EVs can promote tumor survival and growth by transferring oncogenic molecules between tumor cells. Tumor-derived EVs can influence neighboring stromal cells, such as endothelial cells and fibroblasts, promoting tumor growth, angiogenesis, and invasion. EVs contribute to the formation of pre-metastatic niches (PMNs) by creating a favorable environment for metastatic cells. They can promote vascular leakiness, facilitating the arrival of circulating tumor cells at distant sites. Tumor EVs also influence the immune system, modulating immune responses and promoting both pro-tumor and anti-tumor immunity. They can suppress immune cells, including T cells and natural killer cells, and promote the recruitment of immunosuppressive cells like myeloid-derived suppressor cells (MDSCs). EVs can also promote metastasis by transferring miRNAs that regulate gene expression and promote tumor progression. They can influence the tumor microenvironment by reprogramming stromal cells, immune cells, and bone marrow-derived cells. EVs have potential as biomarkers for cancer progression and as therapeutic agents for drug delivery and targeting. They can be directed to specific tissues and used to deliver therapeutic agents such as siRNAs and proteins. Future research is needed to understand the role of different EV subpopulations in cancer progression, the mechanisms of EV-mediated reprogramming, and the potential of EVs as diagnostic and therapeutic tools. In vivo studies are essential to analyze the role of EVs in cancer progression and to develop effective strategies for their use in cancer treatment.Extracellular vesicles (EVs) secreted by tumor cells play a critical role in intercellular communication, contributing to both primary tumor growth and metastatic progression. These EVs, including exosomes, microvesicles, and oncosomes, contain bioactive molecules such as nucleic acids, proteins, and lipids that can alter the function of recipient cells. They promote angiogenesis, coagulation, immune modulation, and tissue remodeling, supporting tumor progression and metastasis. Clinically, EVs may serve as biomarkers and therapeutic targets for cancer progression, particularly for predicting and preventing future metastatic development. EVs are involved in various physiological processes, including coagulation, immune regulation, and development. They facilitate bidirectional communication between the embryo and uterine endometrium, contributing to successful implantation. EVs also play a role in pregnancy by promoting an immune-tolerant microenvironment. In cancer, EVs can promote tumor survival and growth by transferring oncogenic molecules between tumor cells. Tumor-derived EVs can influence neighboring stromal cells, such as endothelial cells and fibroblasts, promoting tumor growth, angiogenesis, and invasion. EVs contribute to the formation of pre-metastatic niches (PMNs) by creating a favorable environment for metastatic cells. They can promote vascular leakiness, facilitating the arrival of circulating tumor cells at distant sites. Tumor EVs also influence the immune system, modulating immune responses and promoting both pro-tumor and anti-tumor immunity. They can suppress immune cells, including T cells and natural killer cells, and promote the recruitment of immunosuppressive cells like myeloid-derived suppressor cells (MDSCs). EVs can also promote metastasis by transferring miRNAs that regulate gene expression and promote tumor progression. They can influence the tumor microenvironment by reprogramming stromal cells, immune cells, and bone marrow-derived cells. EVs have potential as biomarkers for cancer progression and as therapeutic agents for drug delivery and targeting. They can be directed to specific tissues and used to deliver therapeutic agents such as siRNAs and proteins. Future research is needed to understand the role of different EV subpopulations in cancer progression, the mechanisms of EV-mediated reprogramming, and the potential of EVs as diagnostic and therapeutic tools. In vivo studies are essential to analyze the role of EVs in cancer progression and to develop effective strategies for their use in cancer treatment.