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Life sciences · Journal article
Cancer Drug Resistance · October 28, 2026
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Drug resistance in cancer is shaped not only by tumor-cell-intrinsic mutations but also by spatially organized microenvironmental states. PLA2G2A, encoding group IIA secreted phospholipase A2 (sPLA2-IIA), is usually discussed as an inflammatory lipid enzyme; however, its cancer relevance depends strongly on cellular source, localization and disease stage. This Review uses a compartment-resolved framework that annotates four domains - source, spatial niche, linked biochemical output and functional or therapy-response phenotype - and separates PLA2G2A-specific mechanistic evidence from evidence for therapy or immune resistance. Several cancer studies provide PLA2G2A-specific functional evidence for invasion, proliferation/stemness, non-catalytic signaling or T-cell dysfunction, but direct demonstration that PLA2G2A changes response to a defined anticancer therapy remains sparse. The pancreatic ductal adenocarcinoma cancer-associated fibroblast study provides the strongest resistance-proximal immune-functional evidence, whereas mucinous colorectal extracellular vesicles, ovarian ascites, invasive-front fibroblasts, treatment-remodeled stroma and prognostic signatures require more direct therapy-response validation. Gastric and intestinal epithelial data further caution that PLA2G2A may accompany differentiation, invasion restraint, antimicrobial defense or barrier protection. We therefore argue against treating PLA2G2A as a universal oncogenic target. Instead, it should be advanced as a mechanism-matched biomarker or therapeutic hypothesis only when compartment, biochemical-output, functional and perturbational evidence converge.