ArticleCell death discovery2026
Apatinib inhibits synovial sarcoma progression and angiogenesis via VEGFR2-mediated AKT/FOXO3A and ERK1/2/FOXM1 signaling pathways.
Article in Cell death discovery, 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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Abstract
Synovial sarcoma (SS) is a highly aggressive soft-tissue malignancy with limited therapeutic options for advanced disease. Here, we report that apatinib, a selective VEGFR2 tyrosine kinase inhibitor, exerts potent antitumor and anti-angiogenic activity in SS. In SS cell lines, apatinib reduced cell viability, induced G1 phase arrest, and triggered both apoptosis and autophagy. Apatinib further suppressed the metastatic phenotype by inhibiting cell migration, invasion, and EMT, while simultaneously reducing VEGF expression and impairing endothelial tube formation. Mechanistically, apatinib suppressed the VEGFR2/AKT/FOXO3A and ERK1/2/FOXM1 axes in tumor cells, thereby restraining proliferation and angiogenic signaling, and directly impaired endothelial function via the VEGFR2/AKT/eNOS/NO pathway in HUVECs. In vivo, apatinib markedly suppressed xenograft tumor growth and modulated the corresponding signaling pathways. Collectively, our findings identify apatinib as a promising therapeutic agent that disrupts interconnected survival and angiogenic networks in SS.
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