ArticleJournal of translational medicine2026
SFRP2 drives aerobic glycolysis and tumor progression in ovarian cancer by transcriptional upregulation of PTK2B.
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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Abstract
backgroundOvarian cancer is a highly lethal gynecologic malignancy, with metabolic reprogramming being a key contributor to its progression and therapeutic resistance. Although Secreted Frizzled-Related Protein 2 (SFRP2) has been implicated in various cancers, its functional role and molecular mechanisms in ovarian cancer, particularly in regulating metabolic pathways, remain poorly defined.
methodsBioinformatic analyses of GEO (GSE66957) and TCGA-OV datasets were performed to assess SFRP2 expression and its prognostic correlation. Immunohistochemistry (IHC) on a human ovarian cancer tissue microarray was used for clinical validation. SFRP2 was knocked down or overexpressed in ovarian cancer cell lines (HEY and SK-OV-3) using lentiviral shRNA vectors. Functional assays (CCK-8, colony formation, apoptosis, migration) and metabolic assays (glucose consumption, lactate/ATP production, ECAR/OCR) were conducted. The mechanistic link between SFRP2, transcription factor CEBPA, and downstream target PTK2B was investigated using co-immunoprecipitation (Co-IP), nuclear-cytoplasmic fractionation, chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays. Rescue experiments were performed both in vitro and in vivo (xenograft mouse models).
resultsSFRP2 was significantly overexpressed in ovarian cancer tissues and cell lines, and high SFRP2 expression correlated with advanced disease and poor patient survival. SFRP2 knockdown suppressed cell proliferation, colony formation, and migration, while promoting apoptosis. Mechanistically, SFRP2 interacted with the transcription factor CEBPA, promoted its nuclear translocation, and enhanced its occupancy at the PTK2B promoter, thereby driving PTK2B transcriptional activation. This SFRP2/CEBPA/PTK2B axis further activates the AKT/mTOR signaling pathway, upregulating key glycolytic enzymes. Importantly, inhibiting glycolysis with 2-DG or knocking down PTK2B effectively reversed the oncogenic effects of SFRP2 both in vitro and in vivo.
conclusionOur findings identify a novel SFRP2/CEBPA/PTK2B signaling axis that drives aerobic glycolysis and malignant progression in ovarian cancer, highlighting SFRP2 and PTK2B as potential prognostic markers and therapeutic targets.
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