{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n G protein‐coupled receptor 87 (GPR87) is emerging as an important cell surface mediator in cancer, functioning as a receptor that can be activated by ligands such as lysophosphatidic acid (LPA) and belonging to a subfamily related to the P2Y receptors."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In several cancer settings—including pancreatic, bladder, lung, and squamous cell carcinomas—it is frequently overexpressed, where its activation promotes cell proliferation, survival, angiogenesis, and resistance to apoptosis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": " Notably, RNA interference–mediated knockdown of GPR87 in bladder and pancreatic cancer models leads to reduced cell viability and enhanced apoptotic responses, underscoring its role in tumor cell survival."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "5"}]}, {"type": "t", "text": " In addition, DNA damage studies have revealed that p53 directly upregulates GPR87, which in turn mediates p53-dependent prosurvival signaling, highlighting a feedback mechanism that may enable cancer cells to resist genotoxic stress."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "7"}]}, {"type": "t", "text": " Epigenetic regulation also appears to be involved, as chromatin remodeling via H3.3 deposition can activate GPR87 transcription in lung cancer, suggesting potential prognostic value."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}]}, {"type": "t", "text": " Moreover, GPR87 has been independently identified as a component of glycolysis-related prognostic signatures in head and neck squamous cell carcinoma and as a predictor for increased recurrence in bladder cancer, supporting its candidacy as a novel therapeutic target."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ken-ichi Tabata, Kiyoshi Baba, Akira Shiraishi, et al. 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