VCAN (Versican)

VCAN limits T cell trafficking and effector function and its proteolysis correlates with an effector phenotype of circulating CD8+ T cells, greater tumor infiltrating lymphocytes and improved clinical outcomes with this immunotherapy-based clinical trial treatment.

CS/DS content increased 3.4-fold in A549 sEVs, while the ratio of the two monosulfated disaccharides changed 2-fold. These findings demonstrate the utility of N-glycoproteomics and GAG profiling for sensitively characterizing molecular differences between sEVs derived from different cell culture models, thereby providing a foundation for future EV biomarker studies.

CAFs with elevated VCAN levels promoted the proliferation, migration, and invasion of high-stemness adenocarcinoma cells via the MDK-NCL and MIF-CD74-CD44 signaling pathways, while also enhancing immune evasion and self-renewal. These results position VCAN as a potential new therapeutic target for STAD.

In contrast, from days three to seven post-infection, there was significant upregulation of avidin (AVD), a biotin-binding protein, and versican (VCAN), which is linked to tissue remodelling and inflammation. These findings correlate with the disease's progression from initial liver infection to widespread bacterial presence, suggesting value as host biomarkers for effective SLD monitoring and the development of targeted therapies.

The role of syndecan 1 is a bit more complex; namely, the nature of its role is context dependent. In this narrative review article, the roles of PGs in prostate cancer progression and therapy resistance are discussed in more detail.

Furthermore, PGs appear to modulate the tumour immune landscape, are involved in the development of metastatic niches, and underlie signalling pathways like Wnt or TGFβ in a subtype-dependent manner, extending their translational prospects and therapeutic utility. PGs, taken together, seem to be major modulators of BC, with particular relevance for precision medicine.

In silico analyses provided a rationale behind the different biological activities of the two compounds. These findings highlight the potential of non-chelating glycoconjugated arylsulfonamides to treat pathologies characterized by excessive ADAMTS5 activity.

The combined treatment promotes hair follicle growth by activating the Wnt/β-catenin pathway through STMN1 upregulation. BoNT/A in conjunction with PRP facilitates hair follicle growth and reconstruction through STMN1 protein modulation and Wnt/β-catenin pathway activation.

T1 was essential for effective TGF-β signalling, V1 upregulation, and subsequent renal fibrosis.

This work revealed that several GP-CFs from Decay-accelerating factor (CD55), Versican (VCAN), Carboxypeptidase Z (CPZ)and Mucin 16 (MUC16) have the potential to distinguish PDAC NATs from Ts, with an area under the curve (AUC) of 1 in the validation cohort. These data demonstrate that CF glycoproteins may associated with PDAC development and progression and have potential as candidate biomarkers for clinical decision-making.

Multivariate Cox regression analysis showed that non-surgical patients (hazard ratio &lsqb;HR]: 4.03 (1.26-12.82); P = 0.02), whose tumors presented necrosis (P < 0.001), high HS expression (P = 0.02), and low biglycan expression (HR: 2.68 &lsqb;1.16-6.18]; P = 0.02) had significantly worse overall survival rates. We concluded that the expression of GAGs and PGs in the ECM affects the plasticity of MM, modifies its phenotype, and facilitates both its progression and resistance to treatment.

Further cell migration, invasion, qPCR and western blot assay shows that visfatin promoted esophageal cancer cell migration by decreasing miR‑3613‑5p expression and subsequently increasing vascular endothelial zinc finger 1/versican production. Thus, the visfatin/miR‑3613‑5p axis may be a promising target for inhibiting esophageal cancer cell migration and invasion.