PRSS3 (Serine Protease 3)

In LPS-treated cells, HDAC7 knockdown reduced TNF-α, IL-1β, IL-6 levels, and apoptosis, and increased cell viability, which also reversed by Nur77 knockdown. HDAC7 may inhibit Nur77 to exacerbate ARDS by upregulating Igkv14-126, IGLC2, Prss3b, and downregulating Ccdc50 and Chchd7, offering new targets for ARDS treatment.

A significant reduction in gastric cancer tumor growth was observed in mice undergoing combination therapy with LNPs and fluorouracil (5-FU) compared to mice receiving 5-FU alone. Anti-TMPRSS4-siRNA loaded LNPs may be considered a promising therapeutic modality for gastric cancer.

In a macrophage-tumor-fibroblast co-culture model, knockout of SPP1 in macrophages led to reduced expression of lipid-metabolism related genes and disrupted tumor-promoting interactions. Together, these results indicate that CRC growth in the brain is sustained by a specific cellular organization with immunosuppressive multicellular interactions.

This methylation pattern was associated with reduced survival rates and further validated its correlation with tumor metastasis in an independent cohort (n = 243). Our study elucidates that methylation-regulated alternative splicing contributes to phenotypic heterogeneity in GC, highlighting its potential advantage over differentially expressed genes in improving stratification strategies for precision oncology.

Furthermore, PRSS3 knockdown improved chemosensitivity to paclitaxel and doxorubicin and alleviated resistance to trastuzumab in BRCA cells. Our findings uncover a novel PRSS3-mediated mechanism underlying ferroptotic evasion in BRCA. Targeting the PRSS3-PAR2-ERK1/2 axis may offer therapeutic potential, with PRSS3-V1 serving as a valuable biomarker for BRCA subtype stratification.

The importance of the secreted serine protease, S1 family member PRSS22 in tumor progression is highlighted. It shows promise as a biomarker for CC prognosis and as a target to prevent tumor spread by inhibiting its enzymatic activity.

Furthermore, analyses of other structures suggest that dynamic sampling of closed states with analogous allosteric cryptic pockets appears widespread among S1 serine proteases. These observations point to a potentially generalizable strategy to achieve selective inhibition, offering broad implications for drug development targeting serine proteases in cancer and other diseases.

These findings suggest inflammation and specific biomarkers may drive pain and fatigue during chemotherapy. Further preclinical models or clinical cohorts are needed to validate these results and explore potential implications for targeted interventions to reduce symptom burden in patients with colorectal cancer.

This study underscores the versatility and potential of synthetic nanobody engineering in the development of highly selective protease inhibitors, paving the way for their consideration as drug candidates for clinical development.

Our results shed light on the potential connections between ribosome biogenesis-related molecular characteristics and clinical features, the tumor microenvironment, and clinical drug responses. The research underscores the critical role of ribosome biogenesis in the progression and treatment resistance of pancreatic cancer, offering valuable new perspectives for prognostic evaluation and therapeutic response prediction in pancreatic cancer.

PRSS3 is significantly upregulated in LUAD and can be used as a marker for LUAD diagnosis and prognosis assessment. Further study of PRSS3 could provide valuable insight into the mechanisms underlying the occurrence and progression of LUAD.

This research suggests that PRSS3 holds great potential as a target for solid cancer treatment. This cycle-based approach to antibody screening shows potential because it can be broadly applied to cancer and other challenging diseases.