SDC4 (Syndecan 4)

The data point to hormone-independent proliferative programs and immune-modulating fibroblast subtypes as key contributors. These insights broaden our understanding of tumor biology and may guide the development of targeted, less invasive treatments for young patients.

Further studies have shown that AGO promotes SDC4-CTF lysosomal degradation and reduces the production of sEVs. In summary, our findings demonstrate that AGO blocks SDC4-Syntenin interaction and inhibits sEVs biogenesis, providing a new pharmacological ligand for targeting SDC4.

This transformative process, wherein Scissor+ cells acquire malignant features, highlights novel mechanisms of cancer progression. These findings provide deeper insights into hepatocarcinogenesis and offer potential avenues for targeted and personalized therapeutic strategies.

Notably, the natural compound epigallocatechin gallate (EGCG) effectively blocks this IL1β-NFκB-SDC4 axis by inhibiting NFκB nuclear translocation, thereby attenuating SDC4 upregulation and subsequent EC cell proliferation. Our findings establish SDC4 as a critical molecular link between inflammation and EC progression, and highlight EGCG as a potential therapeutic candidate targeting this pathway.

This study highlights the novelty of our pipeline in integrating RNA-seq data to identify robust intercellular communication networks in AD. By prioritizing consistent interactions across datasets, we provide insights into AD pathology that inform experimental validation and therapeutic development.

Computational analysis suggests that the high-risk group is potentially sensitive to targeted drugs such as ZM447439. Furthermore, in vitro experiments confirmed that FN1 silencing significantly suppresses the migration and proliferation of PTC cells. This study systematically deciphers the functional adaptive reprogramming during PTC LNM, providing novel insights and tools for LNM prediction and targeted therapy.

BACH1-driven CM-TAMs activate TBLCs via the ANGPTL4-SDC4 signaling axis, promoting stemness and cholesterol accumulation, ultimately driving malignant progression in chordoma. These findings uncover a previously unrecognized tumor-immune-metabolic interaction and suggest potential therapeutic targets for this disease.

VWF, PDGFRA and FCN1 were stably expressed in both groups, suggesting the existence of a conserved homeostatic regulatory network. In conclusion, this study reveals the cross-tissue functional heterogeneity of cell types shared by CRC and SP, suggests a set of potential pervasive regulators, and provides new perspectives for understanding the systemic effects of tumors and the microenvironmental mechanisms of sarcopenia.

To assess the generalizability of this finding, we deconvolved bulk RNA-sequencing data using single-cell RNA-sequencing data as a reference to examine the relationship between receptor expression levels and overall survival (OS). This analysis revealed that high SDC4 expression in cancer cells is associated with poor OS in HGSOC patients.

Emerging data reveal its crosstalk with HER2/FGFR1 pathways and identify K48-ubiquitination as a therapeutic resistance mechanism. These findings position domain-selective GPNMB targeting as a promising precision oncology strategy.

Hp-stimulated CAFs played a significant role in promoting tumor proliferation in Hp + GC. Targeting its "TLR/miR-148a-5p/CALD1/collagen VI" pathway was a promising method to ease the collagen-rich microenvironment and inhibit the proliferation of GC cells. Furthermore, miR-148a-5p agomir might serve as a safer and more efficacious chemotherapeutic sensitizer for patients with Hp + GC.

Elevated IL-17 expression and nuclear localization of β-Catenin may contribute to the progression of OLP toward dysplastic transformation, with this pattern being most evident in the erosive subtype. These findings suggest that a combined immunohistochemical panel may support risk stratification in OLP, although validation in larger, prospective cohorts is warranted.