Endocrine tumors arise from highly differentiated hormone-secreting cells and are characterized by strong hormone dependence, high metabolic activity, and marked phenotypic plasticity. During tumor progression and therapeutic intervention, endocrine tumor cells can adapt to adverse microenvironmental conditions and treatment pressure through remodeling of differentiation states, reprogramming of signaling pathways, and metabolic adaptation. Regulated cell death (RCD) is a key determinant of cell fate and an important mediator of anticancer treatment responses, while also being closely linked to tumor plasticity. In this review, we summarize the major forms of RCD in endocrine tumors and their crosstalk, with a focus on how hormone and metabolic signaling shape the RCD network and influence tumor plasticity. Current evidence suggests that endocrine signals, nutrient-sensing pathways, and organ-specific metabolic stress regulate multiple forms of RCD, including apoptosis, ferroptosis, autophagy-dependent cell death, and inflammatory cell death, thereby influencing the death threshold of tumor cells and contributing to therapy resistance, dedifferentiation, and invasive behavior. We also discuss emerging therapeutic strategies targeting RCD, as well as potential biomarkers and clinical stratification approaches. A better understanding of the interaction between RCD and endocrine tumor plasticity may help shift the current therapeutic concept from simply inducing tumor cell death to limiting maladaptive plasticity, thus offering new opportunities to overcome therapeutic resistance and dedifferentiation.