Extracellular vesicles (EVs) play a significant role in intercellular communication and are involved in various physiological and pathological processes, including cancer progression. EVs can mediate nonapoptotic regulated cell death (RCD) forms such as ferroptosis, pyroptosis, and necroptosis, which are distinct from apoptosis and contribute to tumor development and resistance to therapy. This review highlights the biological functions and mechanisms of EVs in mediating these nonapoptotic RCD forms and their potential clinical applications in cancer diagnosis and therapy. EVs can deliver various cargoes, including lipids, proteins, and nucleic acids, to regulate tumor progression. For instance, EVs can induce ferroptosis, a iron-dependent form of oxidative cell death, by facilitating the removal of iron from cells, thereby preventing cell death in tumor suppression. Pyroptosis, a form of inflammatory cell death, is regulated by caspase activation and the release of proinflammatory cytokines. Necroptosis, a form of regulated necrosis, is controlled by RIPK1, RIPK3, and MLKL, leading to the rupture of the plasma membrane and the release of intracellular contents. EVs can influence the crosstalk between local and remote recipient cells, affecting immune suppression, premetastatic niches, immune surveillance, and tumor immune microenvironment. The review also discusses the potential of EV-based drug delivery systems in targeting cell death regulators to enhance therapeutic efficacy. Overall, the understanding of EV-mediated nonapoptotic RCD forms and their mechanisms holds promise for advancing cancer diagnosis and treatment.Extracellular vesicles (EVs) play a significant role in intercellular communication and are involved in various physiological and pathological processes, including cancer progression. EVs can mediate nonapoptotic regulated cell death (RCD) forms such as ferroptosis, pyroptosis, and necroptosis, which are distinct from apoptosis and contribute to tumor development and resistance to therapy. This review highlights the biological functions and mechanisms of EVs in mediating these nonapoptotic RCD forms and their potential clinical applications in cancer diagnosis and therapy. EVs can deliver various cargoes, including lipids, proteins, and nucleic acids, to regulate tumor progression. For instance, EVs can induce ferroptosis, a iron-dependent form of oxidative cell death, by facilitating the removal of iron from cells, thereby preventing cell death in tumor suppression. Pyroptosis, a form of inflammatory cell death, is regulated by caspase activation and the release of proinflammatory cytokines. Necroptosis, a form of regulated necrosis, is controlled by RIPK1, RIPK3, and MLKL, leading to the rupture of the plasma membrane and the release of intracellular contents. EVs can influence the crosstalk between local and remote recipient cells, affecting immune suppression, premetastatic niches, immune surveillance, and tumor immune microenvironment. The review also discusses the potential of EV-based drug delivery systems in targeting cell death regulators to enhance therapeutic efficacy. Overall, the understanding of EV-mediated nonapoptotic RCD forms and their mechanisms holds promise for advancing cancer diagnosis and treatment.