CTSD (Cathepsin D)

Treatment further normalized membrane-bound ATPase activities, reduced tumor-associated enzyme markers (5'-nucleotidase, γ-glutamyltransferase, cathepsin D), regulated apoptosis-related endpoints (BAX, BCL-XL, P53; caspase-3) and improved mammary tissue histoarchitecture. Collectively, these findings support PEGylated β-galactosidase as a well-tolerated macromolecular candidate with in vivo antitumor potential mediated primarily through redox restoration and apoptosis regulation.

Baicalin enhanced the sensitivity of BC cells to cisplatin by inhibiting autophagic flux through lysosomal activity suppression. This study provides a potential botanical drug candidate for chemosensitization during BC chemotherapy.

Enzymatic assays revealed that AMA02194 selectively inhibited Mtb-CAβ1 and β2 with inhibition constants of 8.2 and 39.7 nM, respectively, and displayed stronger potency than the reference inhibitor acetazolamide under the tested conditions...Host gene expression profiling provided a lung-tissue expression context and computationally predicted associations for genes including CTSD, GSTP1, and NFE2L2, which are annotated to immune and redox-related functions. Overall, the results support AMA02194 as an isoform-selective inhibitor of Mtb β-carbonic anhydrases at the enzyme level and provide a computational framework for further investigation of porphyrin-based modulators in tuberculosis-related studies.

Collectively, our study establishes a novel regulatory axis, ZNF384/KIF13B/STT3A/CTSD/THBS1, essential for macrophage-hepatocyte crosstalk during MASLD progression and providing potential therapeutic targets for the treatment of MASLD.

Functional enrichment demonstrated coordinated impacts on extracellular matrix organization, inflammation, and metabolic adaptation. This work provides a multicompartment degradomic resource that captures proteolytic remodeling in melanoma lung metastasis and establishes a foundation for future functional and translational studies.

The CSTD simulation reduced 114 vials but resulted in a 2.76% increase in total cost (R$ 125,789.92 vs. R$ 122,416.55). An increase in treated patients (256 vs. 245) and completed cycles (1118 vs. 1074) was observed.ConclusionAlthough direct cost reduction was not achieved, CSTD use may eliminate waste, expand patient access, and optimize public healthcare resources.

The results of this research provide value to the field of proteomics as a large-scale, reproducible, and hypothesis-generating plasma dual-omics reference dataset. This study was not designed to establish diagnostic biomarkers, to assess clinical discriminative performance, or to imply causal mechanisms. Instead, by emphasizing reproduciblilty across independent cohorts, we provide a plasma dual-omics reference dataset that captures coordinated immune and lipid metabolic alterations associated with chronic liver disease severity. These data provide a framework and resource for future studies researching risk stratification, therapeutic monitoring, and mechanistic validation in chronic liver disease.

In parallel, IFN-β activates STAT1/STAT3 to upregulate cathepsin D expression, whereas TGF-β enhances GSDME phosphorylation by downregulating PPP1R3G, a regulatory subunit of protein phosphatase 1. Using lipid-hybrid nanoparticle-delivered mRNA technology, the tri-cytokine cocktail demonstrated therapeutic efficacy against orthotopic PDAC in mice and PDX models, highlighting its translational potential for PDAC patients.

Our study offers a foundational framework for using PGRN in glioma diagnosis and prognosis. The potential of PGRN as both a diagnostic and prognostic biomarker was identified suggesting novel avenues for targeted therapeutic strategies in glioma management.

P=N/A, N=20, Recruiting, Mayo Clinic | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2025 --> Dec 2026

Our study identified specific proteins as potential NMIBC biomarkers and drug targets. The identified proteins, particularly those linked to tumor recurrence and staging, warrant further validation to assess their clinical utility in NMIBC diagnosis, prognosis, and treatment strategies.

Notably, genetic deletion or pharmacological inhibition of CTSD using pepstatin A prevents immune escape and enhances anti-PD-1 efficacy. These findings identify CTSD as a key mediator of immune evasion in MSS CRC and support the development of a combination therapy comprising CTSD inhibition and anti-PD-1 immunotherapy.