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<p>Osteosarcoma (OS) is a highly aggressive malignant bone tumor predominantly affecting adolescents and children. Extracellular vesicles (EVs) significantly contribute to the progression of osteosarcoma by promoting intercellular communication via the transportation of biomolecules and activation of signaling pathways. However, the specific role of tenascin-C (TNC) transmitted by EVs in osteosarcoma remains poorly understood. In this study, we reanalyzed mass spectrometry data of osteosarcoma-derived EV proteins from public databases. EVs were isolated and characterized using standard protocols. The expression levels of EV-derived TNC (EVs-TNC) were measured by western blot or enzyme-linked immunosorbent assay. Functional assays were used to elucidate the role of EVs-TNC in promoting OS malignancy. Transcriptome sequencing was conducted to identify downstream effectors of EVs-TNC. Our results revealed elevated circulating EVs-TNC concentrations in OS patients versus healthy controls. Furthermore, EVs-TNC derived from OS cell lines (SJSA-1 and 143B) were internalized by MG-63 cells, enhancing their proliferative and migratory capabilities. Mechanistically, EVs-TNC was found to regulate angiotensin II receptor type 1 (AGTR1) expression, suggesting a potential signaling pathway involved in OS progression. This study highlights the role of EVs-TNC in promoting OS proliferation and migration, indicating that targeting EVs-TNC may offer a novel treatment strategy for osteosarcoma.</p>

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Tenascin-C-enriched extracellular vesicles contribute to osteosarcoma progression via regulation of the angiotensin II receptor type 1 pathway

  • 期刊论文

  • 发表日期：

    2025年11月4日

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  • Lei Wang,
  • Kai Liu,
  • Lihua Lyu,
  • Zongsheng Yin

摘要

Osteosarcoma (OS) is a highly aggressive malignant bone tumor predominantly affecting adolescents and children. Extracellular vesicles (EVs) significantly contribute to the progression of osteosarcoma by promoting intercellular communication via the transportation of biomolecules and activation of signaling pathways. However, the specific role of tenascin-C (TNC) transmitted by EVs in osteosarcoma remains poorly understood. In this study, we reanalyzed mass spectrometry data of osteosarcoma-derived EV proteins from public databases. EVs were isolated and characterized using standard protocols. The expression levels of EV-derived TNC (EVs-TNC) were measured by western blot or enzyme-linked immunosorbent assay. Functional assays were used to elucidate the role of EVs-TNC in promoting OS malignancy. Transcriptome sequencing was conducted to identify downstream effectors of EVs-TNC. Our results revealed elevated circulating EVs-TNC concentrations in OS patients versus healthy controls. Furthermore, EVs-TNC derived from OS cell lines (SJSA-1 and 143B) were internalized by MG-63 cells, enhancing their proliferative and migratory capabilities. Mechanistically, EVs-TNC was found to regulate angiotensin II receptor type 1 (AGTR1) expression, suggesting a potential signaling pathway involved in OS progression. This study highlights the role of EVs-TNC in promoting OS proliferation and migration, indicating that targeting EVs-TNC may offer a novel treatment strategy for osteosarcoma.