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Publication

The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability.

Cell reports | 2023

Glioblastoma (GBM) is the most common and aggressive primary brain malignancy. Adhesion G protein-coupled receptors (aGPCRs) have attracted interest for their potential as treatment targets. Here, we show that CD97 (ADGRE5) is the most promising aGPCR target in GBM, by virtue of its de novo expression compared to healthy brain tissue. CD97 knockdown or knockout significantly reduces the tumor initiation capacity of patient-derived GBM cultures (PDGCs) in vitro and in vivo. We find that CD97 promotes glycolytic metabolism via the mitogen-activated protein kinase (MAPK) pathway, which depends on phosphorylation of its C terminus and recruitment of β-arrestin. We also demonstrate that THY1/CD90 is a likely CD97 ligand in GBM. Lastly, we show that an anti-CD97 antibody-drug conjugate selectively kills tumor cells in vitro. Our studies identify CD97 as a regulator of tumor metabolism, elucidate mechanisms of receptor activation and signaling, and provide strong scientific rationale for developing biologics to target it therapeutically in GBM.

Pubmed ID: 37938973 RIS Download

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Associated grants

Agency: NCATS NIH HHS, United States
Id: UL1 TR001445
Agency: NCI NIH HHS, United States
Id: P30 CA016087
Agency: NINDS NIH HHS, United States
Id: R01 NS124920
Agency: NIGMS NIH HHS, United States
Id: T32 GM136542
Agency: NCI NIH HHS, United States
Id: R21 CA263402
Agency: NIBIB NIH HHS, United States
Id: R01 EB028774
Agency: NINDS NIH HHS, United States
Id: R21 NS126806
Agency: NINDS NIH HHS, United States
Id: R01 NS102665
Agency: NCI NIH HHS, United States
Id: R01 CA251669
Agency: NCI NIH HHS, United States
Id: R21 CA246457

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