TEAD3 (TEA Domain Transcription Factor 3)

Molecular genetic studies identified a novel EWSR1::TEAD3 gene fusion. This is the first reported case of a peritoneal mesothelioma harboring this fusion.

Our findings indicate that while molecular weight and TPSA influence CNS penetration, efflux transporter interactions are more predictive of brain exposure. MSC-4070 represents a promising candidate for targeting TEAD-driven tumors in the central nervous system.

The identified genetic markers related to pain provide a biological basis for the profound physical suffering. At the same time, the robust DALYs and YLDs data quantify the devastating impact on mental health, particularly highlighting the significant burden of depression and anxiety.

In lung cancer xenograft studies, representatives from both substance classes demonstrated monotherapeutic antitumor activity. For one selected example, the combination effect with the KRASG12C inhibitor sotorasib was demonstrated in vivo.

We define a TEAD3-driven melanoma subtype reliant on SCFA metabolic reprogramming and M2 macrophage crosstalk. The GAS6-TYRO3 axis and Mmut-mediated methylmalonic acid accumulation represent actionable targets. Combining myeloid-GAS6 ablation with immune checkpoint blockade overcomes therapy resistance, offering a precision strategy for high-risk melanoma.

In summary, 16 hub genes and 6 location-related genes enhance our understanding of the potential molecular mechanisms underlying CRC spatial heterogeneity. Furthermore, GZMB and IER3 might be potential targets for CRC therapy.

Pharmacological inhibition of YAP/TAZ-TEAD interaction by Verteporfin significantly decreased tumor cell growth, whereas specific inhibition of TEAD3 did not impact cell proliferation but affected sterol/cholesterol biosynthetic and metabolic processes. This study contributes to a better understanding of the role of Hippo effectors in glioblastoma pathophysiology. These transcription factors, particularly TEAD3, could potentially serve as therapeutic targets, especially considering recent data on cholesterol homeostasis in glioblastomas.

Combining the consistent results from colocalization analysis, differential APA analysis, and survival analysis, we provide novel evidence for the role TUBB APA regulation in NSCLC and identified potential upstream regulators. Overall, our study profiled the APA regulation and highlighted the substantial role of APA in NSCLC carcinogenesis and prognosis in East Asian populations.

Consequently, we identified a novel hydrogen-bonding site and discovered C-2, which effectively binds to this site, as confirmed by X-ray crystallography. Furthermore, C-2 exhibited stable pharmacokinetic properties and demonstrated impressive efficacy in a mouse xenograft model.

Moreover, RNA-seq and Gene Set Enrichment Analysis (GSEA) revealed that the YAP signature genes such as CTGF, CYR61, and ANKRD1 are significantly downregulated by HC278 treatment. Overall, HC278 serves as a valuable chemical tool for unraveling the intricate biological roles of TEAD1 and TEAD3 and holds the potential as a lead compound for developing targeted therapy for TEAD1/3-driven pathologies.

Subsequently, YAP was bound to TEAD3, leading to the transcription of KLF4. Overall, our findings revealed that EphA2 can enhance the stemness of OSCC cells, and this study identified the EphA2/KLF4 axis as a potential target for treating OSCC.

Our results suggest that the LATS2-YAP1-BIRC3/5 axis participates in the RE cell proliferation and promotes rumen growth during the preweaning period.