CTGF (Connective tissue growth factor)

In a fibroblast subpopulation, upregulation of phosphatase and tensin homolog signaling, indicated an antifibrotic effect of MFGE8. In conclusion, our study reaffirms the profibrotic effects of TGF-β1 and highlights MFGE8 as a novel player in equine endometrial fibrosis with our results suggesting an antifibrotic effect of MFGE8.

Opportunities abound for development of targeted therapies for management of ameloblastoma. Potential candidates are inhibitors of BRAF/MEK and smoothened (SMO) gene/HH pathways, interruption of the TGF-β-Cancer-associated fibroblast axis, anti-angiogenic strategies, immune checkpoint blockade, and RANKL-directed therapy.

Pharmacologic blockade of TGF-α with Fepixnebart, a first-in-class ligand-neutralizing antibody targeting TGF-α and previously not tested in oncologic indications, significantly inhibited early lymph metastasis of EGFR⁺ tumor cells. Furthermore, EGFR overexpression resulted in increased cellularity in tumor-draining lymph nodes and reduced CD8⁺ T-cell representation. Together, these findings reveal a role for the TGF-α/EGFR axis in lymph metastasis and propose a rationale for repositioning EGFR-targeted therapies toward targeting early metastatic spread and immunomodulation in breast cancer.

In aggregate, these findings may contribute to a better understanding of disease pathophysiology and help elucidate the role of potentially clinically relevant TGF-β signaling. This is particularly significant given the clinical use of agents targeting TGF-β-signaling such as luspatercept, as well as the emergence of several CCN2-targeting therapies currently undergoing clinical or preclinical evaluation with promising results.

The identified gene signatures may serve as candidates for hypothesis generation and provide a computational framework to prioritize biomarkers and therapeutic targets in cervical cancer. However, these findings are based on in silico analyses and require experimental and clinical validation before translation into practice.

This article integrated the action targets and regulated biochemical processes of effective components of TCM targeting the Hippo signaling pathway in anti-tumor activities and discovered that flavonoids, terpenoids, glycosides, and other effective components of TCM and TCM formulas can regulate the Hippo signaling network, with the most significant mechanisms being the intervention of YAP/TAZ nuclear-cytoplasmic shuttling, restoration of the activity of Hippo core kinases, and blocking of crosstalk between pathways. Taking the Hippo pathway as the research object not only provides a new perspective for explaining the scientific connotation of TCM in anti-tumor activities but also lays a theoretical foundation for the development of new TCM drugs based on Hippo pathway-targeted therapy.

RT-qPCR assays demonstrated that Peptide-4 significantly downregulated the mRNA expression levels of CTGF and CYR61. In conclusion, the data demonstrated that the peptide-4 may serve as a promising candidate to disrupt the YAP-TEAD4 interaction and enhance biological activity in AML-related cellular models.

Clear cell renal cell carcinoma (ccRCC) is predominantly treated with anti-angiogenic therapies (AATs), such as sunitinib and axitinib. CTGF may thus serve as both a predictive biomarker and a therapeutic target. These findings support further investigation of CTGF inhibition as a strategy to overcome AAT resistance and improve treatment outcomes in ccRCC patients.

We found that high-viscosity treatment promotes P-gp (ABCB1) expression, enhancing doxorubicin (DOX) chemoresistance...The inhibition of YAP transcriptional activity suppressed the high viscosity-induced increases of P-gp mRNA and protein levels, supporting the YAP dependence of P-gp upregulation. Reducing tumor viscosity may provide new insights for overcoming drug resistance in clinical settings.

Moreover, NSUN2 is transcriptionally activated by the YAP-TEAD2 complex, forming a positive feedback loop that promotes tumor growth and metastasis, a process effectively suppressed by m5C inhibitors both in vivo and in vitro. Furthermore, our presented findings suggest that NSUN2 promotes tumor growth and metastasis by increasing ALYREF/YBX1-mediated YAP expression in NSCLC and effective inhibition of m5C modification might provide a potential treatment strategy for NSCLC.

H. pylori infection induces persistent ICTM after eradication. Infection-driven iCAF differentiation contributes to epithelial malignant transformation and a potential immunosuppressive microenvironment, linking to gastric carcinogenesis. Our findings underscore the critical role of ICTM transformation, highlighting the need to improve ICTM for post-H. pylori eradication therapies, and indicate that specific iCAF subtypes represent promising intervention targets.

CTGF induction in LSECs may play an upstream role in the fibrogenesis of CH. The integrin αV-YAP-CTGF axis in LSECs could be a potential therapeutic target for CH.