TL;DR
The findings suggest that CAFs-derived CCL11 may represent a potential therapeutic target for PCa, largely through regulating CDK5 expression.
It is hypothesised that the CXCR4 High -CAF transcriptome profile is compatible with a biologically plausible theory of transition between paracrine and autocrine regulatory modes and inflammatory cell states, and suggests a possible shift from TGF-β-dependent to CXCR4-mediated regulation of CXCL12.
CAV1 is identified as a fibroblast-associated gene linked to stemness- and ferroptosis-related signatures and promoting bladder cancer progression by activating the LIF-STAT3 signaling axis.
This study delineates a novel CAF-driven immunosuppressive pathway in HCC, where CD147+ CAFs enhance tumor cell PD-L1 expression and susceptibility to immune checkpoint blockade via a TIMP2/MMP2/IL-6 axis.
A VEGFA-associated functional CAF state promotes gastric cancer organoid growth and chemoresistance through paracrine signaling, highlighting the CAF-VEGFA axis as a potential therapeutic target.
This work identified p38α MAPK (p38α; MAPK14) as a key regulator of inflammatory CAF activation and collagen remodeling and implicates it as a central mediator of stromal remodeling and therapeutic resistance in pancreatic cancer.
Serving as a highly prevalent malignant tumor, lung adenocarcinoma (LUAD) is frequently associated with the establishment of an immunosuppressive tumor microenvironment during its initiation and progression, where M2-polarized macrophages exert pivotal effects. NCAPD3 acts as an oncogenic driver in multiple tumors; how...
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