TGFBI (Transforming Growth Factor Beta Induced)

Both cases showed classic DFSP morphology and diffuse CD34 expression. These findings expand the molecular landscape of DFSP and illustrate convergent mechanisms of PDGFR-β activation achieved through diverse yet functionally equivalent genomic rearrangements.

TGFBI knockdown or GDF15 inhibition results in a decrease in functional proteins associated with stemness maintenance, which suppresses bladder CSCs' self-renewal and effectively improves the efficacy of chemotherapy. Together, these findings demonstrate the pivotal role of TGFBI in BLCA's stemness maintenance and BLCA progression, highlighting that the inhibition of the TGFBI/GDF15 axis is a potential therapeutic strategy for the amelioration of cancer chemotherapy.

In an external validation cohort, an area under the curve (AUC) of 0.922 for low-grade ccRCC detection and 0.874 for high-grade ccRCC detection was achieved, respectively, using urinary EVs. Furthermore, integrating single-cell sequencing data revealed that SERPINA1 and VEGFA in low-grade ccRCC, and APOC1 and TGFBI in high-grade ccRCC, were derived from tumour-associated macrophages, whereas NDUFA4L2 originated from cancer cells in both low- and high-grade ccRCC.

Elevated PDGF-B reversely stimulates TGFBI production in macrophages, which creates a positive feedback loop. This TGFBI-mediated interaction between HSCs and macrophages remodels the profibrotic microenvironment to promote liver fibrosis, identifying a potential therapeutic target.

PCL upregulated oncogenic proteins and activated oncogenic signaling pathways. DEPs detectable in the liver and serum indicate potential FALD biomarkers. These findings offer insights into the pathophysiology of FALD and hepatocarcinogenesis and support the development of novel diagnostic and therapeutic strategies.

This study provides insights into the molecular mechanisms underlying PAAD and establishes a theoretical foundation for the development of CAF-targeting therapeutic strategies.

Further, our study showed that intervention with the administration of an miR-21 mimic in WT livers effectively improves insulin sensitivity, steatosis, fibrosis, Tgfbi expression, and tumor burden in CD-HFD conditions. These findings indicate that miR-21 could serve as an effective strategy to delay or prevent liver disease in HFD environments.

THBS1, carried by ovarian cancer-derived exosomes, promotes M2 polarization of TAMs by modulating TGFBI expression. The subsequent M2 polarization of TAMs contributes to the establishment of an immunosuppressive tumor microenvironment, thereby facilitating disease progression. Consequently, targeting the exosome-mediated signaling axis between cancer cells and macrophages represents a promising avenue for developing novel therapeutic interventions.

Finally, blocking BIGH3 in a TGFβ-induced fibrosis model led to reduced PRO-C3 levels, demonstrating that BIGH3 is local mediator of pathological TGFβ signaling. This highlights that BIGH3 may be implicated in TGFβ-induced fibrosis and underscore the potential for treatment of pathological fibrotic processes by inhibiting BIGH3 in patients with elevated PRO-C3 levels.

This study elucidates the tumor-endothelial interactions mediated by STC2 and ITGA5 in smoking-associated LSCC, emphasizing their roles in tumor progression and vascular permeability. These findings suggest potential prognostic biomarkers and therapeutic targets to improve the clinical management of smoking-associated LSCC.