GPX7 (Glutathione Peroxidase 7)

This study constructed and validated a metabolism-driven prognostic model. The model enables prognostic stratification of LGG patients and links high-risk scores to metabolic dysregulation and an immunosuppressive microenvironment characterized by M2 macrophage enrichment, based on multi-omics data. Mechanistic exploration indicates this association is particularly pronounced in myeloid cells, predominantly within metabolism-related M2 macrophage subpopulations. Furthermore, computational analysis suggests differences in drug sensitivity between risk groups and identifies potential therapeutic compounds, providing clues for future exploration of therapeutic strategies targeting metabolic-immune interactions.

Mechanistically, glutamine metabolism shapes the OS tumor microenvironment by modulating immune-evasion and angiogenic cues, underscoring its dual role in metabolic adaptation and immune-metabolic crosstalk. Collectively, this study establishes a single-cell-anchored, glutamine-coupled state in OS, introduces an externally validated prognostic tool with translational promise but modest discriminative power, and positions MSMO1 as a metabolic-signaling node warranting further mechanistic and in-vivo investigation.

Regarding ferroptosis markers, GPX7 knockdown increased acyl-CoA synthetase long-chain family member 4 and reduced solute carrier family 7 member 11; moreover, GPX7 knockdown increased Fe2+ levels; the above findings indicated that GPX7 knockdown promoted ferroptosis in human osteosarcoma cells. GPX7 knockdown inhibits osteosarcoma cell growth, invasion, and migration while facilitating oxidative stress and ferroptosis.

Through bioinformatics analysis, we identified several oxidative stress-related hub genes and signaling pathways in OKC which was related to IL-1β expression.

Our study demonstrates that GNF-5837 reduced the expression of ageing markers by upregulating GPX7, suggesting it could serve as a potential treatment for IVDD.

Current standard therapies, including surgery, radiotherapy, and temozolomide (TMZ) chemotherapy, are limited by drug resistance and the blood-brain barrier...eQTL-MR analysis identifies GBM-associated differentially expressed genes and constructs a protein-protein interaction (PPI) network.Integrating pQTL data from the deCODE database, pQTL-MR, and colocalization analyses validated the therapeutic potential of GPX7 and CXCL10.These findings provide new perspectives on GBM biology and suggest actionable targets for therapy. Despite limitations due to sample size and population-specific data, this study highlights GPX7 and CXCL10 as promising candidates for further investigation and lays the foundation for targeted GBM treatments.

This comprehensive analysis of missense mutations in GPx7 and GPx8 provides critical insights into their impact on protein structure and stability, contributing to a deeper understanding of the roles of somatic mutations in cancer development and progression. These findings can inform more precise clinical diagnostics and targeted treatment approaches for cancers.

Elasticnet model tuning on individual marker expression revealed top tumor predictive markers, including FKBP10, ATP1A2, NT5DC2, UGT3A2, PYCR1, CKB, GPX7, DNMT3B, GSTP1, and OXCT1. These findings indicate that an activated metabolic transcriptional program, potentially influencing epigenetic functions, is observed in hepatoblastoma tumors and confirmed at the single-cell level.

Moreover, the knockdown of RRM1 suppresses the progression of HCC cells. In this study, we developed a robust prognostic model for predicting the prognosis of HCC patients based on GMAGs, and identified RRM1 as a potential therapeutic target for HCC.

GPX7 was identified as a more promising biomarker for glioma. We provide important insights into the treatment and prognosis of gliomas.

Altogether, this study reveals the fundamental role of the SNPs of antioxidant defense genes in COVID-19 progression and susceptibility of individuals to this virus. In addition, different responses of COVID-19 patients to antioxidant defense system enhancement drugs may be due to presence of these SNPs in different individuals.