SERPINB3 (Serpin family B member 3)

A panel comprising seven key IPF genes was identified, which may have diagnostic and prognostic value for IPF. A comprehensive analysis of the Dgidb database revealed potential drugs that may be antitumor agents against IPF, such as Lygodii Spora, Smilacis Glabrae Rhizoma, and Aloe.

Together, these data indicate that TNBC exhibits co-existing immune activation and immune-suppressive features. The identified epithelial and stromal signatures represent candidate biomarkers that may inform future studies of immune regulation and therapeutic stratification in TNBC.

Our findings reveal a disease-defining autoantibody repertoire in paraneoplastic pemphigus that corresponds with clinical manifestations and holds high potential for early cancer detection in patients with blistering disease.

Clinically, SERPINB3 is highly expressed in human LUAD specimens and co-localizes with SENP3 and NPM1. Our work establishes SENP3 as a bona fide endogenous substrate of SERPINB3 and delineates a novel sumoylation-dependent oncogenic axis in LUAD, offering potential therapeutic targets for this malignancy.

Consensus clustering was utilized to classify PC samples into two HH signaling-related subtypes: HRGcluster A and HRGcluster B. In contrast with HRGcluster A, HRGcluster B has an earlier clinical stage, better outcome, less active level of HH signaling, higher infiltration level of CD8+ T cells and B cells, and a greater likelihood of benefiting from immunotherapy and gemcitabine chemotherapy...In vitro assays further indicated that DCBLD2 knockdown downregulates HH signaling and inhibits the proliferation, migration, and invasion of PC cells. In conclusion, this study reveals that HH signaling characteristics in PC and DCBLD2 regulate HH signaling to drive PC progression, providing new perspectives and theories for the diagnosis and treatment of PC.

Our findings indicated that the rondom froest model based on five autoantibodies might help identify preclinical and early-stage PC.

To this end, we further developed a metal-organic framework (MOF) loaded with both copper ions and MEK inhibitor, which significantly triggers tumor-specific cuproptosis and enhances antitumor immunity. In summary, SERPINB3 serves as a predictive biomarker to inform therapeutic strategies targeting cuproptosis, thereby establishing a novel paradigm for cancer immunotherapy that integrates metal biology, targeted therapy, and immune modulation.

Recombinant Serpinb3a, the mouse ortholog, enhances re-epithelialization in vitro and accelerates wound closure and collagen remodeling in vivo. These findings reveal a physiological function for SerpinB3 in epithelial repair and suggest that its expression in cancer, chronic wounds, and inflammatory diseases may reflect reactivation of a conserved wound response program-positioning SerpinB3 as a compelling therapeutic target.

Finally, in pilot experiments conducted on stimulated saliva from a patient with a lung cancer nodule, we detected altered content or selective presence of proteins involved in lung carcinogenesis, such as serpin B3 or the proteins S100A14 and aldoketoreductase-A1, respectively. While acknowledging that these findings require further validation, we believe that the use of saliva and related proteomic analyses may contribute to the identification of potential early lung cancer biomarkers, which could hopefully improve clinical management of the tumor and patient survival.

Due to its multifaceted involvement in liver disease, PAR2 is emerging as a key therapeutic target in this clinical context. This review aims to summarise current knowledge on PAR2's role in MASLD and its potential as a therapeutic target.

These findings show distinct gene expression profiles and modulated pathways in AA and CA PDACs, supporting development of race-based therapeutic targets.

Increased ROS induces the expression of hypoxia-inducible factor 1α (HIF1α), which in turn transcriptionally activates serpin family B member 3 (SERPINB3) to enhance TNBC stemness, thus leading to TNBC progression and cisplatin resistance. Collectively, these findings identify TMEM65 as a vital oncogene of TNBC, unveil its regulatory mechanisms, and shed light on its potential role in TNBC therapy.