FURIN (Furin, Paired Basic Amino Acid Cleaving Enzyme)

Colorectal cancer (CRC) remains one of the most lethal malignancies worldwide, with 5-fluorouracil (5-Fu) as a mainstay of treatment...Collectively, these findings demonstrate that furin promotes CRC progression and chemoresistance through a positive feedback loop with TGF-β that sustains ERK activation. Targeting furin, alone or in combination with TGF-β/ERK inhibitors, may offer a promising therapeutic strategy for CRC.

Additionally, mTOR overexpression reduced uncleaved prM and intracellular viral RNA while increasing furin levels in DENV-infected cells. These findings highlighted a DENV maturation process, which is fine-tuned by the RRM2-mTOR-mediated pathway.

Targeted inhibition of furin and related convertases represents a promising avenue for broad-spectrum antiviral interventions. Collectively, current evidence positions furin as a central node at the intersection of viral pathogenesis, host genetic variability, and translational therapeutic potential.

During this process, the Cou excimers were formed and induced a red shift in the fluorescence emission, validating the feasibility of RF-Cou in efficient excimer imaging of furin-overexpressing tumor cells. We expect that our findings will highlight the potential of stimuli-responsive small molecular peptide probes to advance excimer-based imaging platforms, particularly for enzyme-specific cell imaging and therapeutic monitoring.

Using ▵Fur293 and derivatives that express mutant forms of furin, we confirm the importance of furin in the PE RIT intoxication pathway and show that furin trafficking has a significant impact on RIT efficacy. Our data support the hypothesis that furin acts as a transporter during RIT intoxication and suggest furin as a target for modification to improve the effectiveness of RITs.

Furthermore, we constructed a liver fibrosis mouse model by CCl4-induced method and found that forced expression of Furin caused alleviation of liver fibrosis in CCl4-induced mice. Our findings provide a new clue for understanding liver fibrogenesis and highlight the therapeutic potential of Furin for hepatic fibrosis.

Further Mendelian randomization analysis confirmed the causal relationship between FURIN and LUAD development. These findings provide novel biomarkers for the prognosis evaluation of LUAD based on cuproptosis and disulfidptosis mechanisms and offer a theoretical basis for targeting FURIN in LUAD treatment.

This pattern of dysregulation was distinct from the broader trends observed in a variety of cancer types through bioinformatic analysis of publicly available transcriptomic datasets, where FURIN expression was predominantly upregulated compared to other PCs. Further bioinformatic investigations revealed a correlation between PC gene expression and cancer phenotype diversity, suggesting a potential link between the loss of normal PC gene expression patterns and the progression of HPV infections toward malignancy.

In summary, our work highlights the translational potential of furin-inhibited CAR-Ms as a potent cellular therapy to mitigate macrophage exhaustion within the tumor environment. By capitalizing on macrophage-mediated antitumor responses, these findings pave the way for the development of second-generation CAR-M therapeutic strategies tailored for solid tumors.

P=N/A, N=800, Recruiting, Shanghai Changhai Hospital; Changhai Hospital

Disruption of these disulfide linkages with the prodomain enabled Activin-A binding to cognate type II receptors independently of proteolytic maturation. Stepwise proteolytic maturation is a novel mechanism to control Activin-A protein interactions and signaling.

Canine mesothelin exhibits molecular and biological characteristics akin to human mesothelin. It could serve as a vital biomarker for diagnosing canine mesotheliomas, applicable to both tissue- and effusion-based samples.