SEMA3A (Semaphorin 3A)

HOXD13 orchestrates 3D enhancer-promoter contacts activating VEGFA, SEMA3A, and CD73, which remodel vasculature and elevate immunosuppressive adenosine. Consistently, HOXD13-induced tumor growth is reversed by combined VEGFR and adenosine receptor (AdR) inhibition, revealing a dual pro-angiogenic and immunosuppressive HOXD13 axis with therapeutic relevance.

Papain exhibits antileukemic effects in vitro, associated with mitochondrial-mediated apoptosis, altering cell-cycle progression, suppressing Sema3A expression, and modulating inflammatory responses. These findings suggest that papain may represent a candidate for further preclinical investigation in leukemia models.

Transcriptome analysis revealed that combination treatment decreased the expression of pro-proliferative and migratory genes (e.g., PDPN, CDH3), while increasing the expression of anti-migratory (RND3) and pro-apoptotic genes (e.g., XAF1, SEMA3A). Thus, combination treatment significantly reduces tumor cell proliferation and migration; however, further studies on surviving cells are needed.

Among inflammatory cytokines, TNF-α levels increased dose-dependently (∗∗∗∗p < 0.0001), while IL-6 and IL-10 showed no significant alterations. Collectively, These findings indicate that the synthesized thiazole compound exerts selective cytotoxicity toward prostate cancer cells via mitochondria-mediated apoptosis and inflammatory signaling modulation.

Because PTPRD functions are pathway-specific and shaped by mini-exon usage or redundancy with other family members (PTPRS/PTPRF), domain- or ligand-selective interventions represent plausible therapeutic strategies. Elucidating its full ligand repertoire, substrate landscape, and structural basis for allosteric regulation will be critical for converting this versatile receptor from a mechanistic curiosity into a tractable target for neurodevelopmental, neuropsychiatric, and metabolic disorders.

Prognostic core genes (SHH: EMILIN3, CD163; GP3/GP4: SEMA3A, TULP1) predicted survival outcomes and demonstrated diagnostic specificity. This first comprehensive TME atlas of MB subtypes elucidate mechanisms of immunosuppressive niche formation and provides actionable core targets for precision immunotherapy.

Serum Sema3A is decreased and FGF-23 is increased in CP patients, which is closely related to periodontal parameters and disease severity, and combination evaluation has a high value in estimating the severity of CP patients.

Meanwhile, the PI3K-Atk anti-apoptotic pathway and the ECM-receptor interaction pathway were inhibited during both infections. This study explored the pathogenic mechanism of STB based on proteomics and compared its differences with E.coli bone infection, providing new insight into the treatment of STB.

This transcriptional repression subsequently attenuates TGF-β signaling by diminishing Smad2/3 phosphorylation, a critical regulatory node of this pathway. Collectively, our findings elucidate a previously unrecognized tumor-suppressive mechanism wherein HIC2 inhibits GBM progression through modulation of the SEMA3A-TGF-β signaling axis.

These results suggest that while NRP-1 has potential as a biomarker, its prognostic utility as a standalone factor remains limited. Further studies are warranted to validate these findings in larger cohorts and to explore the molecular mechanisms underlying NRP-1's role in PCa.

The findings highlight the potential of hBN-HA hybrid hydrogels as a next-generation therapeutic strategy for OA, offering dual benefits of inflammation suppression and cartilage regeneration. Given their superior efficacy over HA alone, these biomaterials represent a promising translational approach that could be further explored for clinical applications in OA treatment.

Besides, Sema-3A expression is dramatically reduced by microRNA (miR)-145-5p and miR-497-5p, demonstrating the inhibitory impact of these microRNAs on the Sema-3A expression. Altogether, these findings suggest the crucial roles of Sema-3A in ARDs pathogenesis and introduce it as a promising therapeutic tool for treating these diseases.