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Life sciences · Journal article
Frontiers in Pharmacology · October 21, 2026
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Background Obesity-related metabolic dysfunction and chronic inflammation are well-established drivers of the carcinogenesis and progression of endometrial cancer (EC). Eicosapentaenoic acid (EPA) is a long-chain omega-3 polyunsaturated fatty acid that has previously demonstrated broad anti-inflammatory and anti-tumor properties in various cancer models. In this study, we evaluated the anti-tumorigenic effects of EPA in EC cell lines and in a genetically engineered mouse model of endometrioid EC. Methods Human EC cell lines, KLE and HEC-1B, were used to evaluate the effects of EPA alone or in combination with carboplatin on cell proliferation, invasion, cell cycle profile, stress response, and apoptosis. An LKB1 fl/fl p53 fl/fl genetically engineered mouse model of endometrioid EC was used to examine the effects of EPA on endometrial tumor growth. Results EPA treatment markedly suppressed cell proliferation and colony formation in a dose-dependent manner. Mechanistically, EPA induced G1 cell cycle arrest, promoted cellular stress, and activated cleaved caspases, while inhibiting cell adhesion and migration. These phenotypes were accompanied by robust inhibition of the AKT/mTOR signaling axis and activation of MAPK-mediated stress pathways. Inflammatory signaling was similarly attenuated, as evidenced by reduced TNF-α–induced COX-2 expression and decreased phosphorylation of NF-κB. Importantly, EPA synergized with carboplatin to enhance anti-tumor efficacy. Combination treatment produced stronger suppression of cell proliferation and invasion, increased apoptotic activity, and downregulation of key survival and oncogenic regulators, including phosphorylated AKT, Bcl-2, β-catenin, and CDK4. Four weeks of EPA administration significantly reduced endometrial tumor burden in both obese and lean mice, accompanied by decreased expression of Ki-67, Bcl-xL, β-catenin, and COX-2 in endometrial tumor tissues. Conclusion EPA exerts potent anti-tumor activity in EC through coordinated modulation of oncogenic signaling, inflammatory pathways, cellular stress responses, and apoptosis. Moreover, its ability to enhance carboplatin sensitivity highlights the potential of EPA as an adjuvant therapeutic candidate for EC and warrants further investigation in preclinical models of EC.