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• W2920171213 abstract "// Pierre Vandenberghe 1 , Marine Delvaux 1 , Perrine Hagué 1 , Christophe Erneux 2 and Jean-Marie Vanderwinden 1 1 Laboratory of Neurophysiology, Faculty of Medicine, Université Libre de Bruxelles, Brussels, Belgium 2 IRIBHM, Faculty of Medicine, Université Libre de Bruxelles, Brussels, Belgium Correspondence to: Christophe Erneux, email: cerneux@ulb.ac.be Jean-Marie Vanderwinden, email: jmvdwin@ulb.ac.be Keywords: KIT; PDE3A; cancer; verteporfin; drug repurposing Received: December 10, 2018      Accepted: February 03, 2019      Published: March 05, 2019 ABSTRACT Despite the introduction of tyrosine kinase inhibitors, gastrointestinal stromal tumors (GIST) resistance remains a major clinical challenge. We previously identified phosphodiesterase 3A (PDE3A) as a potential therapeutic target expressed in most GIST. The PDE3 inhibitor cilostazol reduced cell viability and synergized with the tyrosine kinase inhibitor imatinib (Gleevec™) in the imatinib-sensitive GIST882 cell line. Here, we found that cilostazol potentiated imatinib also in the imatinib-resistant GIST48 cell line. Cilostazol induced nuclear exclusion, hence inactivation, of the transcriptional co-activator YAP, in a cAMP-independent manner. Verteporfin, a YAP/TEAD interaction inhibitor, reduced by 90% the viability of both GIST882 and GIST48 cells. Our results highlight the potential use of compounds targeting PDE3A or YAP in combined multitherapy to tackle GIST resistance." @default.
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• W2920171213 date "2019-03-05" @default.
• W2920171213 modified "2023-10-18" @default.
• W2920171213 title "Potentiation of imatinib by cilostazol in sensitive and resistant gastrointestinal stromal tumor cell lines involves YAP inhibition" @default.
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• W2920171213 doi "https://doi.org/10.18632/oncotarget.26734" @default.
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