PRDX2 (Peroxiredoxin 2)

Additionally, PRDX2 silencing inhibited growth of U87MG cells and increased the level of reactive oxygen species. Furthermore, such modulation reduced susceptibility to CONA, suggesting that this compound exerts its effect on cell viability at least partially through PRDX2 inhibition.

This study revealed that Prdx1, Prdx2, Prdx4, and Prdx5 were elevated in depression models, which might relate to the occurrence of neuroinflammation, coupled with upregulation of oxidative stress responses. This study provided new strategies for the treatment of depression.

Finally, we found that there are 14 traditional Chinese medicines targeting PCa with PRDX4, among which 5 have statistical differences, and Shi Liu Zi may be the best targeted traditional Chinese medicine drug. This study found that PRDX4 is highly expressed in PCa, which may promote the phenotypic progression of PCa cells and has high clinical value.

Across multiple in vivo and in vitro models, PRDX2 inhibition restores metabolic homeostasis, reduces tumor initiation, and selectively impairs HCC cell survival. These findings highlight PRDX2 as a promising biomarker and hepatocyte-directed target for chemoprevention, emphasizing the importance of the interplay between metabolism and liver cancer development.

Additionally, we identified four potential drug targets, including PFAS, EIF2S3, EIF6, and NFKB2. Molecular docking analysis suggested that neratinib, a clinically approved drug, could serve as a promising therapeutic agent for GSRCC, offering new avenues for clinical intervention.

The strong correlation of CTC counts with disease progression and survival underscores their clinical relevance as a prognostic biomarker in NSCLC. This approach presents a viable, non-invasive tool for disease monitoring and stratification of NSCLC patients, with potential for integration into clinical practice.

Functional validation reveals that PRDX1/2 overexpression mitigates GLA-mediated apoptosis, establishing their role as critical redox sensors governing cell fate. The findings delineate a ROS-autophagy-apoptosis axis driven by PRDX1/2 targeting, positioning GLA as a novel therapeutic scaffold for RCC treatment.

This study is the first comprehensive analysis of the potential diagnostic and prognostic impact of the PRDXs family in MM, highlighting their significant associations with ferroptosis and the immune microenvironment. These findings provide a strong experimental and theoretical foundation for developing novel therapeutic strategies targeting ferroptosis and immunotherapy in MM.

Furthermore, some proteins such as PRDX2, TFP1, FGG and F13A1 were found to be closely related to CRC progression and metastasis, and have the potential to be biomarkers for CRC. These findings proposed that it is a promising strategy to identify biomarkers from plasma EVs for early detection and disease monitoring of CRC.

Furthermore, POE reduced the expression of pro-inflammatory and pro-coagulant markers (VCAM-1, ICAM-1, TF) and partially reversed TNF-α-induced endothelial activation. These findings suggest that POE exerts anti-angiogenic effects through a multitargeted mechanism, supporting its potential as a natural therapeutic agent for diseases characterized by aberrant angiogenesis.

These mRNA expression patterns and bioinformatic approaches, in combination with clinical variables and trace elements plasma levels, could give an approximation to create a signature to better understand the progression or aggressiveness of ER-positive breast cancer with a simple and cost-effective blood test.

Perturbations studies in HCC cell lines, a CDX mouse model and patient-derived HCC spheroids unraveled that PRDX2 also mediates cancer initiation, cancer cell proliferation and survival through its antioxidant activity. Targeting PRDX2 may therefore be a valuable strategy to prevent HCC development in metabolic liver disease.