TEAD4 (TEA Domain Transcription Factor 4)

Predictive risk scores were developed based on three candidate MDGs, and a nomogram model was built by integrating clinical variables with these scores. This model can provide personalized prognosis prediction and assess drug resistance among individuals with HCC.

Overall, our results elucidated that TEAD4-driven GPX8 suppresses mitochondrial oxidative stress in TMZ-resistant cells through activation of the CTHRC1/p38 MAPK/FOXO3 pathway, which promotes TMZ resistance in GBM cells. These findings suggest that GPX8 may serve as a novel therapeutic target for overcoming TMZ resistance in GBM.

A single-plasmid lentiviral version LV-G-TEAD4(217) was also developed to enable stable transduction and potential in vivo use. Together, these findings demonstrate that G-TEAD4(217) represents a sensitive, specific, and modular reporter platform for analyzing YAP/TAZ transcriptional activity in diverse biological settings.

These findings support the adaptability of UVM lesions and suggest rational combination therapies targeting both primary GNAQ/GNA11-driven oncogenic signals and their compensatory networks as a more effective, personalized treatment approach for advanced UVM.

This study provides the first evidence of the relationship between ovotoxicity and the Hippo signaling pathway in DMBA-induced ovotoxicity in mice. Therefore, our findings suggest that the Hippo pathway could be pharmacologically targeted to regulate DMBA-induced ovotoxicity.

Notably, in a humanized xenograft mouse model, EBVaGC with elevated CD276 levels exhibited resistance to anti-PD1 immunotherapy, while targeting CD276 in combination with PD1 blockade significantly reduced tumor size. Collectively, our findings elucidate the EBNA1-YAP-CD276 axis as a novel mechanism of immune escape in EBVaGC, providing insights for enhanced immunotherapeutic strategies.

Functional enrichment revealed activation of NOTCH, MAPK, PI3K, and TGF-β signaling and enrichment of early and late estrogen-response programs, uncovering a noncanonical role of SMAD9 in TGF-β signaling. Together, these findings delineate the transcriptional and hormonal circuitry underlying thyroid tumorigenesis, providing a regulatory framework for biomarker-driven therapies based on network activity states.

Dual inhibition of YAP1 and TAZ was required to maximally suppress YAP1/TAZ expression and reduce their nuclear accumulation, transactivation of TEAD, and activation of downstream genes. Conclusions These findings show that combined YAP1 and TAZ inhibition holds promise for the treatment of GCPMs, a highly lethal disease with an urgent need for novel treatment options.

Additionally, serum LAMB1 demonstrates superior diagnostic performance compared to the classic HCC marker alpha-fetoprotein. LAMB1 represents a promising therapeutic target for HCC, and also serves as a potential circulating biomarker for liver cancer screening in clinics.

ACTL6A accelerates the progression of NSCLC by modulating the Hippo/YAP signaling axis and influencing TAMs-mediated immune regulation through CSF1.

Through comprehensive analysis, we identified TEAD4 as a key gene in TNBC with high expression specificity. Irinotecan may be a potential targeted drug for TEAD4, offering a new therapeutic strategy for TNBC and potentially improving patient outcomes. Further experimental verification is required.

In colon cancer, we further identified tumor-specific TFs that are more highly activated in tumor cells than in normal epithelial cells, including CEBPG, LEF1, SOX4, TCF7, and TEAD4, which are pivotal in driving malignant transcriptional programs and represent potential therapeutic targets, as corroborated by single-cell sequencing data from multiple sources and in vitro experiments. Our findings provide a comprehensive understanding of the regulatory dynamics underlying carcinomas and offer valuable insights into potential therapeutic interventions.