G6PD (Glucose-6-Phosphate Dehydrogenase)

This study reveals that bile acid metabolism promotes HCC progression by facilitating vascular network formation and establishing an immunosuppressive tumor microenvironment. The bile acid metabolism scoring system may serve as a novel prognostic biomarker and provide a theoretical foundation for developing precision therapeutic strategies in HCC.

SYP restored sorafenib sensitivity in resistant cells through G6PD inhibition. SYP enhances bevacizumab efficacy by targeting angiogenesis, ferroptosis, and G6PD-mediated resistance, providing a rationale for integrating traditional and modern therapies in HCC management. These findings highlight the value of network pharmacology in elucidating TCM mechanisms and support further clinical evaluation.

Importantly, treatment with G6PD inhibitor (G6PDi), a G6PDi reduced aggressiveness of PR KD cancer cells. These findings suggest that targeting G6PD could be a promising therapeutic strategy to suppress the aggressiveness of luminal breast cancer, using low PR expression as a biomarker.

Patients with G6PDd are susceptible to HEV infection. The facilitation of HEV entry and aggravation of oxidative stress may contribute to HEV susceptibility in patients with G6PDd and severe disease.

Importantly, the identification of CSV also provides a rationale for developing CSV-guided delivery systems, enabling targeted silencing of PVTT-associated molecular drivers such as G6PD. Collectively, our findings highlight G6PD+CSV+ CTCs as a dual-function biomarker for both PVTT risk stratification and treatment response monitoring, offering a novel strategy for the precision management of advanced HCC with PVTT involvement.

Induction of G6PD expression in FOXO1-deficient cells mitigates tumor growth inhibition and alleviates ROS level elevation. These results establish a critical role for FOXO1 in the regulation of G6PD during the antioxidative and proliferative processes of cancer cells.

These metabolic changes impaired tumor cell proliferation and sensitized ICC cells to cisplatin, emphasizing the dual therapeutic potential of targeting G6PD to inhibit tumor growth and overcome chemoresistance...Future research should explore the integration of enhancer profiling into precision medicine frameworks and the development of novel enhancer-targeting strategies. These efforts could uncover additional metabolic vulnerabilities and provide effective treatments for this highly aggressive cancer.

Single-cell analysis showed that G6PD and S100A9 were high-expressed mainly in hematopoietic progenitor cells (HPCs) and macrophages. In conclusion, this study screened four key genes based on PMRGs and constructed a risk model to effectively predict the prognosis of HCC, providing novel potential targets and theoretical basis for the molecular subtyping and individualized treatment of HCC.

Furthermore, molecular docking analysis revealed favorable binding interactions between the compounds and key amino acids of the G6PD, reinforcing their potential as a direct enzyme inhibitors. These findings highlight the pivotal role of G6PD in gliomas under hypoxic conditions and support its inhibition as a promising therapeutic strategy.

The results of this study highlight the cytotoxic effects of BPS and consequently its effect on trophoblast viability. The results of NANOG-DNMT1 gene expression related to BPS exposure reinforces our understanding of EDC-induced placental dysfunction.

This study suggests XD as a potential ferroptosis inducer and the potential role of G6PD/PGD/FSP1/DHODH axis in governing ferroptosis sensitivity in HCC.

Furthermore, G6PD and NRF2 expression in PanCancer TCGA samples correlates with patient survival. This work identifies NRF2-PPP dependency as a targetable vulnerability in these difficult-to-treat MPNSTs, particularly in the NF1/CDKN2A-deleted majority.