Findings report the role of GPX3 in immune modulation in gastric adenocarcinoma, suggesting indirect effects on immune responses.
Gastric cancer is a highly prevalent and lethal malignancy worldwide, with its immune microenvironment playing a crucial role in tumor initiation and progression. Among selenoproteins, glutathione peroxidase 3 (GPX3) is an important antioxidant enzyme that has recently attracted attention for its roles in various cancers. However, the function of GPX3 and its impact on the immune microenvironment in stomach adenocarcinoma (STAD) remain insufficiently explored. Deep STAD tissues were more enriched in immune cells compared to superficial tumour tissues, particularly myeloid cells and fibroblasts. GPX3 was predominantly expressed in fibroblasts and myeloid cells, while its expression in T cells was relatively low, with no significant differences across different tumor layers. Moreover, GPX3 exhibited weak correlations with PD-1 and CTLA-4, suggesting that GPX3 may not directly mediate immune evasion via immune checkpoint pathways. These findings characterize the cellular distribution of GPX3 within the STAD immune microenvironment and provide initial insights into its potential regulatory function. Although GPX3 may not directly influence immune checkpoint pathways, its high expression in myeloid cells and fibroblasts suggests that it might indirectly modulate immune responses by regulating the tumour microenvironment. These results lay a theoretical foundation for future research on GPX3 in gastric cancer and its potential as a therapeutic target.
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Shao et al. (2026) studied this question.
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