PLAU (Plasminogen Activator)

In vivo, OSBPL3 silencing significantly attenuated tumor growth and promoted apoptosis. Collectively, these findings identify an OSBPL3-NFE2L2-PLAU-AKT signaling axis that drives glycolytic metabolism and LUAD progression, showing its potential as a therapeutic target.

BA treatment upregulates PLAU gene expression, but this increased PLAU protein subsequently interacts with and inhibited by BA, leading to downstream pathway suppression. It was concluded it could be served as a promising therapeutic strategy for the treatment of PTC.

In CRC, however, SLC46A1 downregulation induces intracellular folate deficiency, triggering locus-specific DNA hypomethylation at the FOS promoter, which activates oncogenic transcription of key downstream effectors (CCND1, BCL2, PLAU), driving tumor progression. The graphical abstract illustrates the differential impact of SLC46A1 on folate metabolism and gene expression in normal versus tumor cells, highlighting its potential as a therapeutic target in CRC.

Thus, we revealed a protease profile (ADAM9, CTSB, MMP7, CTSC, CTSL, MMP9, and PLAU) associated with glioblastoma progression and further demonstrated that CTSL is regulated by IFN-γ in glioblastoma cells. These results establish a link between IFN-γ signaling and protease regulation in glioblastoma.

Finally, we validated the effect of the super-enhancer activity on PLAU and GSDMC expression. Overall, our study identified super-enhancer-based biomarkers for predicting survival and immunotherapy efficacy in colorectal cancer.

These results provide new insights into the biological basis of SARIFAs and suggest therapeutic vulnerabilities related to the plasmin/plasminogen activator system.

This combined model demonstrates high diagnostic accuracy, suggesting that COL3A1, PLAU, and SPP1 may serve as effective early-stage EC biomarkers. The diagnostic model based on these genes shows high accuracy, making it a promising tool for early-stage cancer screening.

Based on bioinformatics analysis, this study identified nine genes significantly upregulated in CAC and associated with prognosis. Allosteric-site mutations in PLAU, SERPINE1, and KDR affect the binding stability of small-molecule drugs (Anacetrapib, LY2090314), suggesting their role in drug response. Four mutation-specific B-cell epitopes (COL1A1R493H, KDRP551S, ICAM1T1259M, KDRT1260M) exhibit enhanced immunogenicity, indicating potential for antibody-based therapy.

The study we conducted establishes the groundwork for comprehending the function of anoikis genes in glioma, and recognizes PLAU as a potential biomarker for glioma.

In summary, these results illustrate that ZC3H13-mediated m6A modification increases PLAU mRNA stability and expression, thereby enhancing OSCC progression. The online version contains supplementary material available at 10.1007/s10616-025-00882-9.

Sarcomatoid component-specific DNA hypomethylation of TSKU, PLAU, PLEKHG4, RPSAP52, XBP1 and TRIM2 was correlated with both recurrence-free and overall survival. These data suggest that the DNA methylation alterations associated with sarcomatoid change may participate in malignant progression and determine patient outcome.

In conclusion, MAPK3, MLLT4, PLAU, and SERPINE1 emerge as promising biomarkers and therapeutic targets for HNSC.