ArticleFrontiers in oncology2026
Inhibition of GPR68 induces ferroptosis in diffuse intrinsic pontine gliomas.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Diffuse Intrinsic Pontine Glioma (DIPG) is a highly aggressive pediatric brainstem tumor with limited treatment options and dismal prognosis. Previously, we showed that Ogremorphin (OGM), a specific GPR68 inhibitor, induced ferroptosis in glioblastoma multiforme (GBM) cells. Given their shared originating cell type, we investigated OGM's efficacy in inducing ferroptosis in DIPG cells, using normal human astrocytes (NHAs) for comparison. Methods: DIPG cell lines (SF7761, DIPG36, DIPG007) and NHAs were evaluated. OGM sensitivity was assessed via CellTiter-Glo viability assays. Ferroptosis markers including glutathione (GSH) levels, lipid peroxidation (BODIPY C11), and qRT-PCR of ATF4 and SLC7A11 were measured. Rescue experiments used liproxstatin-1 for ferroptosis and Z-VAD-FMK for apoptosis. Genetic validation used shRNA knockdown and overexpression of GPR68/ATF4, plus an ATF4 luciferase reporter assay. Results: OGM treatment in N5 media revealed that NHAs were more resistant (LD Conclusions: These findings suggest that GPR68 inhibition is an attractive therapeutic target for DIPG. Notably, GPR68 inhibition mirrors the effects observed in GBM, inducing ATF4-dependent ferroptotic cell death.
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