Apoptosis, ferroptosis, and the autophagy paradox in peritoneal metastasis.

Peritoneal metastasis (PM) correlates with a diminished prognosis. Throughout the progression of PM, programmed cell death (PCD) often functions as the body's defense mechanism to eliminate aberrant malignant cells. Paradoxically, PCD within tumor cell populations also holds the potential to exert a pro-cancer effect by modulating the tumor microenvironment (TME). Apoptosis-mediated innate immune cells may orchestrate the pro-cancer TME and could potentially evade cancer therapy. This discussion delineates the impacts of PCD in PM, particularly focusing on apoptosis, ferroptosis, and autophagy, constituting a "double paradox" process. On one hand, PM is restrained through the removal of cancer cells, while on the other hand, it is propelled by the stimulation of repair and regenerative responses in the TME. Furthermore, the interplay of various PCDs such as cell apoptosis, autophagy, and ferroptosis in PM is explored, alongside a summary of PCD-based anticancer strategies. These insights aim to provide a theoretical basis for the prevention and treatment of PM.