Abstract
Recent advancements in our understanding of cell death mechanisms have progressed beyond traditional apoptosis to encompass various forms of regulated cell death, notably cuproptosis. This copper-dependent cell death occurs when copper interacts with lipoylated enzymes in the tricarboxylic acid cycle, leading to protein aggregation and subsequent cell death. Alongside this, immunosenescence the gradual decline in immune function due to aging has emerged as a significant factor in cancer progression and response to treatment. Innovative strategies that integrate cuproptosis and immunosenescence are showing considerable promise in cancer therapy. By leveraging the altered copper metabolism in cancer cells, cuproptosis can selectively induce cell death, effectively targeting and eliminating tumors. Simultaneously, addressing immunosenescence can rejuvenate the aging immune system, enhancing its capacity to identify and destroy cancer cells. This dual approach creates a synergistic effect, optimizing therapeutic efficacy by directly attacking tumor cells while revitalizing the immune response. Such integration bolsters the defense against cancer progression and recurrence and holds great potential for advancing cancer treatment modalities and improving patient outcomes. This paper delves into the interactions between cuproptosis and immunosenescence, emphasizing their implications for developing innovative cancer therapies.