ArticleOncogene2026
VEGF-C maturation mediated by CircFOCAD-orchestrated CCBE1 and ADAM10 expression in nuclear-cytoplasmic synergy drives lymphatic metastasis.
Article in Oncogene, 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
Lymphangiogenesis is essential for tumor lymphatic metastasis, yet the molecular mechanisms governing the activation of its key cytokine, VEGF-C, remain unclear. Herein, we identified a circRNA, circFOCAD, through VEGF-C maturation-associated multiple transcription sequencing. CircFOCAD is overexpressed in lymph node (LN)-metastatic bladder cancer (BCa) and is associated with poor prognosis. In footpad popliteal LN metastasis and orthotopic BCa models, circFOCAD enhances VEGF-C-dependent lymphangiogenesis and LN metastasis in BCa. Mechanistically, circFOCAD potentiates pro-VEGF-C cleavage by facilitating the expression of CCBE1 and its newly identified partner, the metalloprotease ADAM10. Specifically, circFOCAD promotes ADAM10 promoter H3K9 acetylation by recruiting YBX1. ADAM10 requires CCBE1 as a scaffold, binding at residue R301/R302, to interact with N-terminal propeptide of pro-VEGF-C at residue E58, provoking VEGF-C maturation and sustaining lymphangiogenesis in BCa. Clinically, neutralizing antibodies against CCBE1 and ADAM10 diminished the LN metastatic of BCa in a patient-derived xenograft (PDX) model. Our findings indicate that circFOCAD acts as an initiator of VEGF-C maturation and may represent a promising therapeutic target in LN metastatic BCa.
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