GSTP1 (Glutathione S-transferase pi 1)

Importantly, rescue experiments revealed that concomitant silencing of PYGM partially alleviated the enhanced lipid accumulation induced by GSTM3 deficiency, indicating that PYGM contributes to the steatotic phenotype downstream of GSTM3 loss. Collectively, these findings identify GSTM3 as a critical protective regulator of alcohol-induced hepatic steatosis and reveal a previously unrecognized GSTM3-PYGM axis that modulates lipid metabolism in ALD, suggesting GSTM3 as a potential therapeutic target for the treatment of ALD.

SH may exert its anti-PCa effects by regulating key biomarkers such as GSTP1 and CXCR2, interfering with oncogenic signalling pathways including Rap1, Ras and MAPK, and modulating the infiltration levels of immune cells such as M0/M1 macrophages simultaneously. The online version contains supplementary material available at 10.1007/s40203-025-00511-5.

This study provides a biochemical and structural characterization of weak, competitive inhibition of hpGSTP1-1 by auxins based on combined in vitro and in silico analyses. While the inhibitory potency is limited and unlikely to be pharmacologically relevant at physiological concentrations, the combined in vitro and in silico findings offer valuable mechanistic and structural insight into auxin-GSTP1-1 interactions.

This integrative single-cell and machine-learning study delineates the molecular heterogeneity of LM in ICC and identifies twelve feature genes linking LM with tumor aggressiveness. These findings provide novel insight into LM-driven oncogenic mechanisms and propose CYC1 and other LM-associated genes as potential biomarkers and therapeutic targets for ICC.

Notably, the key polyamine biosynthesis regulator AMD1 was downregulated in both M2 macrophages and dendritic cells in recurrent lesions, paralleling metabolic evidence of altered arginine-polyamine pathways. These findings suggest that recurrent CA involves coordinated metabolic dysregulation across keratinocytes and immune cells, highlighting potential targets for immunometabolic intervention.

In individuals with HCV genotype 4, the interplay of miRNA152, DNMT1, GSTP1, and CDH1 may contribute to the pathogenesis of HCC. These indicators demonstrate potential roles as therapeutic targets and noninvasive prognostic biomarkers for HCV-related liver disease.

Furthermore, we thoroughly discussed emerging research on the physiological functions and mechanisms of GSTP1 in recent years. This review aims to summarize and explore the relationships between GSTP1 genetic polymorphisms and tumors/diseases, its transcriptional regulation, and to highlight other research directions and biological questions.

This integrated computational study identifies a set of candidate genes through which OTA may potentially interact with HCC-associated molecular networks. The robust binding predicted between OTA and the core targets provides a structural basis for these interactions. These findings offer a prioritized list of targets and a theoretical framework for subsequent experimental validation and investigation into OTA's toxicological role in HCC.

Although several DNA repair gene polymorphisms have been explored, findings remain inconsistent and limited by populations and SNPs studied. Larger, well-designed studies with standardized methodologies are needed to confirm these associations and identify genetic markers for predicting high-risk patients for CIO.

Additionally, increased MUC1 levels in circulating sEVs were confirmed by immunoassay (AUC = 0.840 for early-stage HGSOC vs HC; AUC = 0.860 for late-stage HGSOC vs HC, p-value<0.05). In summary, our sEV proteomic analysis of early-stage HGSOC reveals exo-biomarkers associated with early FT lesions, offering a promising avenue for detecting disease while it remains confined to the fallopian tube.

Mechanistically, A3C enhances the expression of the STING1 and its downstream related molecules Caspase-1, IL-18, and IL-1β; upregulates DNA damage-protective genes (GSTP1 and GPX3); and enhances the expression of cell cycle regulator GAS1. This study establishes A3C as a suppressor in PCa, which impedes tumor progression by regulating key molecules involved in cellular inflammation, cell cycle arrest, and DNA damage response.