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Glut3 Addiction Is a Druggable Vulnerability for a Molecularly Defined Subpopulation of Glioblastoma

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Cosset, Erika | Ilmjärv, Sten | Dutoit, Valérie | Elliott, Kathryn | von Schalscha, Tami | Camargo, Maria, F | Reiss, Alexander | Moroishi, Toshiro | Seguin, Laetitia | Gomez, German | Moo, Jung-Soon | Preynat-Seauve, Olivier | Krause, Karl-Heinz | Chneiweiss, Hervé | Sarkaria, Jann, N | Guan, Kun-Liang | Dietrich, Pierre-Yves | Weis, Sara, M | Mischel, Paul, S | Cheresh, David, A

Edité par CCSD ; Elsevier -

International audience. While molecular subtypes of glioblastoma (GBM) are defined using gene expression and mutation profiles,we identify a unique subpopulation based on addiction to the high-affinity glucose transporter, Glut3.Although Glut3 is a known driver of a cancer stem cell phenotype, direct targeting is complicated by itsexpression in neurons. Using established GBM lines and patient-derived stem cells, we identify a subsetof tumors within the ‘‘proneural’’ and ‘‘classical’’ subtypes that are addicted to aberrant signaling from integrinavb3, which activates a PAK4-YAP/TAZ signaling axis to enhance Glut3 expression. This defined subpopulationof GBM is highly sensitive to agents that disrupt this pathway, including the integrin antagonistcilengitide, providing a targeted therapeutic strategy for this unique subset of GBM tumors.

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