CTGF (Connective tissue growth factor)

Hyperuricemia increased risk among CTGF-CC homozygotes, whereas a nonsignificant protective effect was seen among T allele carriers. Monitoring and lowering serum uric acid may help reduce prostate cancer risk in men with the CTGF-CC genotype.

Despite comparable tumor control, the divergent stromal and inflammatory responses may help explain differences in toxicity and long-term outcomes observed clinically. Our findings emphasize the need to consider microenvironmental and stress-related pathways when selecting and optimizing anthracycline regimens for TACE.

Furthermore, prostaglandin E2 (PGE2) was identified as a downstream mediator of NLRP3 signaling, regulating macrophage-myofibroblast communication. Collectively, these findings reveal a pivotal role for the NLRP3-PGE2 axis in mediating macrophage-stromal crosstalk, providing new insight into inflammatory and reparative dynamics within the bovine endometrium.

Mechanistically, OTUD5 functioned as a deubiquitinase, removing the K48 ubiquitin chain from YAP and maintaining protein stability. Functionally, OTUD5 knockdown markedly attenuated HSCs-induced HT-29 cell proliferation and invasion in vitro and tumor growth in vivo. Our results highlight the critical role of OTUD5/YAP feedback loop in stiffness-induced HSC activation, offering a potential therapeutic target for colorectal liver metastasis.

Immunofluorescent double staining was used to examine the co-expression of CD31 in α-SMA-positive CAFs to identify whether the endothelial-to-mesenchymal transition (EndoMT) is involved in the origin, and obvious colocalization was observed. Visium and Visium HD spatial transcriptomics further revealed endothelial cells (ECs) exhibited remarkable co-expression of CAF-specific marker genes and revealed inferred developmental trajectories to CAFs; molecular determinants, including TIMP1, IGFBP7, THBS2, CD74, COL4A1, COL4A2, AEBP1, S100A6, KCTD12, CALD1, IGHG1, SERPINE1, MCL1, MGP, GSTP1, TAGLN, THBS1, and CTGF, were positively correlated with the spatial developmental trajectories of ECs to CAFs; and CTGF exhibited extensive interactions with other common positively correlated molecular determinants and was a highly connected node in the interaction network. ECs that undergo EndoMT may be one of the potential cellular and mechanical origins of CAFs in HCC, and the development of EndoMT may be associated with CTGF.

Loss of CCN2 expression markedly attenuated cell proliferation, migration, invasion, and oxaliplatin resistance compared with control cells...Collectively, these findings suggest that CCN2 functions as a central regulator of stemness and malignant potential in CRC and may represent a promising therapeutic target to prevent recurrence and metastasis. Additional mechanistic studies are warranted to further elucidate the molecular pathways of CCN2 and to validate the role of APOC2 in liver-metastatic CRC stem cells.

In vivo, MAFF overexpression reduced tumor volume and weight, which was accompanied by inhibition of the YAP1 signaling pathway. MAFF suppresses angiogenesis in NSCLC by blocking YAP1 nuclear translocation and downregulating VEGF and CTGF, highlighting its potential as a therapeutic target.

The YAP inhibitor Verteporfin blunted MELK-driven PASMC proliferation and migration, underscoring the central role of YAP/TAZ signaling. Finally, in vivo pharmacological inhibition of MELK by OTS167 markedly reduced right ventricular systolic pressure, hypertrophy, and pulmonary vascular remodeling in Su/H mice, confirming the therapeutic relevance of MELK targeting in PAH. Collectively, these findings identify MELK as a novel regulator of PASMC pathobiology in PAH and suggest that it may represent a potential therapeutic target.

EBF3 transcriptionally activates ACADL and blocks the Hippo/YAP pathway to inhibit BC progression.

Second- and third-line TKIs, such as sunitinib and regorafenib, provide limited benefits, highlighting the urgent need to address resistance mechanisms. These findings uncover a TGF-β1/CCN2/Rack1/PGK1 mechanism linking CAF-mediated metabolic reprogramming to imatinib resistance in GISTs. Targeting CAF-GIST interactions and key metabolic pathways presents a promising therapeutic strategy.

Furthermore, we newly found Wnt family member 5B (WNT5B) expression was regulated by ZEB1, also involved in osteolytic process. In conclusion, YTHDF3 plays an important role in osteolytic metastasis and it may serve as a potential prognostic biomarker and therapeutic target for breast cancer bone metastasis.

Fucoxanthin may attenuate inflammation and angiogenesis in RA by modulating the PPAR-γ/CTGF pathway, suggesting its potential as a therapeutic agent for managing RA.