ArticleTranslational cancer research2026
Orphan G protein-coupled receptor GPR137 regulates ferroptosis by targeting the Wnt/β-catenin pathway in sonic hedgehog-medulloblastoma.
Article in Translational cancer research, 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: The orphan G protein-coupled receptor (GPCR) GPR137 is implicated in the proliferation of various tumor cells. However, its role and underlying mechanisms in medulloblastoma (MB), particularly the sonic hedgehog (SHH) subtype, remain unclear. This study aimed to investigate the function of GPR137 in SHH-MB and its potential regulation of ferroptosis via the Wnt/β-catenin pathway. Methods: A GPR137-knockdown Daoy cell line was constructed using lentiviral shRNA. Cell proliferation, invasion, and colony formation were assessed using Cell Counting Kit-8 (CCK-8), wound healing, and colony formation assays, respectively. Ferroptosis was induced with erastin, and its inhibition was achieved with ferrostatin-1. Key ferroptosis markers, including lipid peroxidation products [malondialdehyde (MDA), 4-hydroxynonenal (4-HNE)], reactive oxygen species (ROS), glutathione (GSH) levels, and labile iron (Fe² Results: GPR137 knockdown significantly inhibited Daoy cell proliferation, invasion, and colony formation. It synergized with erastin to aggravate ferroptosis, leading to increased cell death, elevated levels of MDA, 4-HNE, ROS, and Fe² Conclusions: Our findings demonstrate that GPR137 deletion promotes ferroptosis in SHH-MB cells by inhibiting the Wnt/β-catenin signaling pathway. This reveals a novel regulatory axis in MB and suggests that targeting GPR137 could be a promising therapeutic strategy for SHH-MB.
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