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<p>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.</p>

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Apatinib inhibits synovial sarcoma progression and angiogenesis via VEGFR2-mediated AKT/FOXO3A and ERK1/2/FOXM1 signaling pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月3日

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  • Ruijie Liu,
  • Fengzhen Zhang,
  • Kai Shi,
  • Wenhao Wang,
  • Xuewen Li,
  • Shaobo Lu,
  • Bowen Chen,
  • Dongjin Wu,
  • Changliang Peng

摘要

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.