ArticleJournal of translational medicine2026
Identification of the CYP19A1-GPER1 axis as a critical oncogenic driver in hepatocellular carcinoma via AKT activation.
Article in Journal of translational medicine, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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9 authors.
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Abstract
backgroundHepatocellular carcinoma (HCC) has limited therapeutic efficacy at advanced stages. Lipid metabolism reprogramming drives HCC progression; however, the functional crosstalk between CYP19A1, GPER1, and lipid metabolic dysregulation in HCC remains unclear.
methodsIntegrated analyses of The Cancer Genome Atlas Liver Hepatocellular Carcinoma data were performed. Clinical validation, functional assays, rescue experiments, in vivo xenografts, and molecular docking were conducted.
resultsCYP19A1 was identified as a prognostic hub in HCC, with overexpression correlating with advanced T/BCLC stages (p < 0.05) and poor survival (log-rank p < 0.05). Gene set enrichment analysis linked CYP19A1 to dysregulated lipid metabolism, pro-tumorigenic signaling, and immune infiltration. GPER1 was found to be a critical effector of CYP19A1, mediating its effects on proliferation, migration, invasion, epithelial-mesenchymal transition, and protein kinase B activation. CYP19A1 knockdown reduced tumor burden in vivo, whereas GPER1 overexpression rescued this phenotype.
conclusionThe CYP19A1-GPER1 axis represents a critical oncogenic driver in HCC, providing a mechanistic insight to guide future therapeutic development.
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