Discovery of Pan-TEAD Inhibitors That Disrupt YAP-TEAD Interaction as a Potential Therapy for Gastric Cancers and Mutant KRAS and EGFR Lung Cancers

发现可破坏YAP-TEAD相互作用的泛TEAD抑制剂,有望成为胃癌以及KRAS和EGFR突变型肺癌的潜在疗法

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Abstract

Dysfunction of Hippo signaling resulting in elevated YAP/TAZ-TEAD activity is commonly associated with tumorigenesis and represents a therapeutic target for cancer. Drug resistance is a significant factor undermining the efficacy of cancer therapy. In this study, we identify a class of covalent small molecules with a vinyl sulfone warhead binding to the conserved cysteine of the TEAD and disrupting its interaction with YAP. These compounds (particularly CPD10 and CPD13) strongly inhibit proliferation and colony formation of cancer cell lines with altered Hippo signaling. Moreover, the TEAD dependency of gastric cancer cells enhance their sensitivity to CPD10 and CPD13 treatment. Importantly, the pan-TEAD inhibitors also promote synergistic cell death in EGFR- and KRAS mutant Non-Small Cell Lung Cancer (NSCLC) cells, which may eventually overcome drug resistance associated with the use of FDA-approved compounds. Therefore, we uncover a novel class of vinyl sulfone warhead-bearing pan-TEAD inhibitors with potential for treating gastric and mutant KRAS and EGFR lung cancers.

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