TSSC3 as a potential biomarker in osteosarcoma: implications for angiogenesis

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INTRODUCTION: . Osteosarcoma (OS) is a highly vascularized malignant tumor whose growth and metastasis depend on angiogenesis. Tumor-suppressing STF cDNA 3 (TSSC3) has been identified as a tumor suppressor in OS, but its role and underlying mechanisms in regulating angiogenesis remain unclear. MATERIALS AND: METHODS: . Immunohistochemistry was used to assess the expression of TSSC3, VEGF-A, and CD31 in OS tissues. OS cells that stably overexpressed TSSC3 were established via lentiviral transduction, and conditioned medium from these cells was used to culture human umbilical vein endothelial cells (HUVECs). The proliferation, migration, and tube formation of HUVECs were evaluated using CCK-8, wound healing, Transwell, and tube formation assays. qRT-PCR and Western blotting were conducted to assess VEGFA mRNA and VEGF-A protein levels in TSSC3-overexpressing cells. A xenograft model in nude mice was used to evaluate angiogenesis in vivo, and changes in the Src/ERK pathway were examined by Western blotting. RESULTS: . TSSC3 was downregulated, and VEGF-A was upregulated in OS tissues, both of which were associated with prognosis. Conditioned medium from the TSSC3-overexpressing cells significantly inhibited HUVEC proliferation, migration, and tube formation. In vivo, TSSC3 overexpression led to reduced tumor weight, VEGF-A expression, and microvessel density. Moreover, TSSC3 suppressed VEGF-A synthesis and secretion in a Src/ERK-dependent manner. CONCLUSIONS: . TSSC3 inhibits angiogenesis in OS by downregulating VEGF-A via the Src/ERK pathway, providing a theoretical and experimental basis for anti-angiogenic therapies targeting TSSC3.

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