| Gastric cancer is a highly prevalent malignant tumor of the digestive tract, with chemoresistance and distant metastasis serving as the major bottlenecks in its clinical treatment. Ferroptosis is an iron-dependent form of programmed cell death mediated by the accumulation of lipid peroxides, which is extensively involved in the proliferation, invasion, metastasis and chemoresistance of gastric cancer. As core regulatory modulators of protein function, protein post-translational modifications (PTMs) dynamically govern the stability, activity and intermolecular interactions of key ferroptosis effector proteins via covalent modifications including ubiquitination, phosphorylation, palmitoylation and lactylation, thereby determining the ferroptotic sensitivity of gastric cancer cells. Recent relevant studies have moved beyond the linear research paradigm focusing on single modification and single target, and shifted their focus to the regulatory network of crosstalk among multiple modifications. This paper systematically reviews the regulatory pathways of ferroptosis, elaborates the molecular mechanisms and crosstalk patterns by which various PTMs modulate ferroptosis in gastric cancer, summarizes current research advances and prospects future research directions, and provides theoretical references for developing therapeutic strategies targeting the PTM–ferroptosis axis against gastric cancer. |
