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<p>Exosomal long non-coding RNAs (lncRNAs) play crucial roles in breast cancer progression. However, the mechanisms by which hypoxia-induced exosomes mediate angiogenesis through lncRNAs in the tumor microenvironment remain largely unexplored. In this study, exosomes were isolated and characterized from MDA-MB-231 breast cancer cells under normoxic and hypoxic conditions. Hypoxia-induced exosomes (Hyp-exo) were shown to significantly promote angiogenesis. Microarray analysis revealed that lnc-MTRNR2L12-3 was highly enriched in Hyp-exo compared to normoxic exosomes (NC-exo). Functional studies, both in vitro and in vivo, demonstrated that exosomal lnc-MTRNR2L12-3 derived from hypoxic breast cancer cells substantially enhanced angiogenesis. Mechanistically, PCR array and western blot analysis confirmed that silencing lnc-MTRNR2L12-3 inhibited Src/FAK signaling pathway activation in HUVECs, while hypoxia-induced exosomes effectively rescued this suppression. Overall, hypoxia-induced breast cancer exosomes deliver lnc-MTRNR2L12-3 to endothelial cells, promoting angiogenesis through the Src/FAK signaling pathway. These findings provide new insights into targeting angiogenesis in the tumor microenvironment for breast cancer therapy.</p>

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lnc-MTRNR2L12-3 derived from hypoxic breast cancer cell exosomes facilitates angiogenesis via the Src/FAK signaling pathway

  • 期刊论文

  • 发表日期：

    2025年6月25日

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  • Li Zheng,
  • Juanfen Mo,
  • Xuesong He,
  • Qi Xu,
  • Yi Bao,
  • Jiayuan Wu

摘要

Exosomal long non-coding RNAs (lncRNAs) play crucial roles in breast cancer progression. However, the mechanisms by which hypoxia-induced exosomes mediate angiogenesis through lncRNAs in the tumor microenvironment remain largely unexplored. In this study, exosomes were isolated and characterized from MDA-MB-231 breast cancer cells under normoxic and hypoxic conditions. Hypoxia-induced exosomes (Hyp-exo) were shown to significantly promote angiogenesis. Microarray analysis revealed that lnc-MTRNR2L12-3 was highly enriched in Hyp-exo compared to normoxic exosomes (NC-exo). Functional studies, both in vitro and in vivo, demonstrated that exosomal lnc-MTRNR2L12-3 derived from hypoxic breast cancer cells substantially enhanced angiogenesis. Mechanistically, PCR array and western blot analysis confirmed that silencing lnc-MTRNR2L12-3 inhibited Src/FAK signaling pathway activation in HUVECs, while hypoxia-induced exosomes effectively rescued this suppression. Overall, hypoxia-induced breast cancer exosomes deliver lnc-MTRNR2L12-3 to endothelial cells, promoting angiogenesis through the Src/FAK signaling pathway. These findings provide new insights into targeting angiogenesis in the tumor microenvironment for breast cancer therapy.