ArticleCancer science2025
Novel TEAD1 Inhibitor VT103 Enhances Dabrafenib Efficacy in BRAF V600E Mutated Lung Adenocarcinoma via Survivin Downregulation.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
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Authors and funding
20 authors.
Funding
Abstract
The BRAF V600E mutation is observed in 2% of the patients with lung adenocarcinoma (LUAD), and combination therapy targeting BRAF and mitogen-activated protein kinase (MEK) is the standard treatment for this population. However, acquired resistance inevitably develops, which highlights the need for novel therapeutic strategies. In this study, we established a patient-derived BRAF V600E-mutated LUAD cell line, KTOR81, and investigated the potential of targeting the Yes-associated protein 1 (YAP1)/transcriptional enhanced associate domain 1 (TEAD1) pathway in combination with BRAF inhibition. We observed that the novel TEAD1 inhibitor VT103 enhanced the efficacy of the BRAF inhibitor dabrafenib in KTOR81 cells and xenograft models. The combination of dabrafenib and VT103 downregulated the expression of the antiapoptotic protein survivin, which is transcriptionally regulated by the YAP1/TEAD1 complex, leading to increased apoptosis. Moreover, we used a LUAD tissue microarray to compare the staining patterns of YAP1, TEAD1, and survivin, and examined their association with prognosis. These analyses revealed a strong correlation between YAP1, TEAD1, and survivin expression in LUAD, suggesting the relevance of the YAP1/TEAD1-survivin axis beyond BRAF V600E-mutated cases. While no statistically significant association was observed between survivin expression and prognosis, when limited to driver oncogene-positive patients, high survivin expression was suggested to be associated with poor prognosis. These findings provide preclinical evidence for the efficacy of combining TEAD1 inhibition with BRAF-targeted therapy in BRAF V600E-mutated LUAD and highlight the YAP1/TEAD1-survivin axis as a potential therapeutic target especially in the driver oncogene-positive LUAD patients.
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