Exploring the Potential Value of Modulation of Cell Death in Immunotherapy of Gynecological Tumors

Cell death plays a pivotal role in a multitude of biological processes, including embryonic development, organ maintenance, aging, immune response, and autoimmunity. These processes are underpinned by distinct molecular mechanisms and have significant implications for biological systems. Currently, research on regulatory cell death (RCD) is primarily focused on apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, and autophagy. These pathways have been shown to play a crucial role in regulating the tumor microenvironment (TME) and influencing the clinical outcome of cancer immunotherapy. RCD exerts a dual regulatory effect on TME, releasing intracellular components and regulating the distribution of immune cells. These cells are involved in fine-tuning the antitumor immune response in the TME. The treatment of gynecological tumors frequently presents a challenge due to the lack of immunotherapeutic responsiveness. This review will focus on apoptosis, necroptosis, pyroptosis, ferroptosis, cuproptosis, and autophagy. It will explore how the molecular messengers released during these processes are involved in regulating their complex interactions with tumor tissues as well as with the immune response. It will also analyze the immunological consequences of regulated cell death and its potential impact on the future development of gynecological oncology therapy. By investigating the mechanisms of cell death, we can gain insight into their role in the development of gynecological tumors and potentially identify new therapeutic strategies to enhance the efficacy of existing treatments and advance cancer care.