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<p>High endothelial venules (HEVs) provide another portal for tumour metastasis. However, whether HEVs and other blood vessels exert different effects on tumour escape remains unknown. Here we show that tumour involvement in HEVs is an independent prognostic marker for patients with lymph node (LN)-positive female breast cancer. Tumour cells that spread via HEVs are less immunogenic and more capable of establishing distant metastases than those that spread through non-HEV blood vessels. Mechanistically, the expression of arachidonate 12-lipoxygenase (ALOX12) in HEVs is promoted by tumour-derived semaphorin 3 C (SEMA3C). Reciprocally, ALOX12-derived metabolite 12-hydroxyeicosatetraenoic acid (12-HETE) promotes ADAR1 p150-dsRNA phase separation in tumour cells by selectively binding to ADAR1 p150. Consequently, the immune recognition of dsRNA is reduced because of the increased adenosine-to-inosine (A-to-I) RNA editing in tumour cells. Collectively, our data indicate that a unique lymphatic anatomical structure mediates specific immune evasion of migrating tumour cells.</p>

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Tumour-associated high endothelial venules drive portal-specific immune evasion in lymph nodes via ALOX12

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月11日

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  • Qidong Xia,
  • Jiayao Pan,
  • Xiaoqi Weng,
  • Shunrong Li,
  • Jiaqian Li,
  • Shijian Song,
  • Jiang Li,
  • Boxuan Zhou,
  • Xinwei Liu,
  • Dong-Ming Kuang,
  • Nu Zhang,
  • Jin Jin,
  • Jinting Liu,
  • Zhen Lin,
  • Shubin Yu,
  • Qionglan Tang,
  • Lijuan Bian,
  • Yunjie Zeng,
  • Yu Shi,
  • Yiqing Zheng,
  • Jian-You Liao,
  • Shouping Xu,
  • Shicheng Su

摘要

High endothelial venules (HEVs) provide another portal for tumour metastasis. However, whether HEVs and other blood vessels exert different effects on tumour escape remains unknown. Here we show that tumour involvement in HEVs is an independent prognostic marker for patients with lymph node (LN)-positive female breast cancer. Tumour cells that spread via HEVs are less immunogenic and more capable of establishing distant metastases than those that spread through non-HEV blood vessels. Mechanistically, the expression of arachidonate 12-lipoxygenase (ALOX12) in HEVs is promoted by tumour-derived semaphorin 3 C (SEMA3C). Reciprocally, ALOX12-derived metabolite 12-hydroxyeicosatetraenoic acid (12-HETE) promotes ADAR1 p150-dsRNA phase separation in tumour cells by selectively binding to ADAR1 p150. Consequently, the immune recognition of dsRNA is reduced because of the increased adenosine-to-inosine (A-to-I) RNA editing in tumour cells. Collectively, our data indicate that a unique lymphatic anatomical structure mediates specific immune evasion of migrating tumour cells.