清华大学、浙江大学研究团队在《自然-免疫》发表论文，揭示了循环肿瘤细胞释放的迁移体在抑制癌症转移中的关键作用 1。研究发现，这些迁移体携带肿瘤相关抗原，被抗原呈递细胞摄取后可激活 CD8+ T 细胞，进而抑制转移 1。实验表明，抑制迁移体形成会促进癌症转移，而注射纯化的癌症来源迁移体则可恢复免疫系统对转移生长的抑制作用 1。
与此同时，纽约大学、东京大学研究团队在《自然》发表论文，从代谢角度揭示了胰腺癌肝转移的机制 1。研究表明，胰腺癌细胞通过 CXCL5-CXCR2 信号通路重塑肝细胞，使其为癌细胞提供丝氨酸代谢支持 1。在小鼠实验中，阻断这一信号通路后可减少肝转移并延长生存 1。两项研究分别从免疫和代谢角度揭示了癌症转移的新机制。
Researchers from Tsinghua University and Zhejiang University have identified a novel immune-based mechanism for suppressing cancer metastasis. Publishing in Nature Immunology on September 22, 2026, their study reveals that circulating tumor cells release structures called migrasomes carrying tumor-associated antigens, which activate CD8+ T cells to inhibit metastatic spread 1. The research demonstrates that when antigen-presenting cells internalize these migrasomes, they trigger immune responses that constrain tumor growth at distant sites 1. Notably, blocking migrasome formation accelerates metastasis, while injecting purified cancer-derived migrasomes restores the immune system's ability to suppress metastatic growth 1.
In a complementary discovery, teams from New York University and the University of Tokyo published findings in Nature on September 23, 2026, that address the metabolic foundations of pancreatic cancer liver metastasis 1. Their work shows that pancreatic cancer cells exploit the CXCL5-CXCR2 signaling pathway to reprogram hepatocytes, compelling them to provide serine metabolic support for tumor cells 1. The researchers found that disrupting this signaling pathway substantially reduces liver metastasis and extends survival in mice 1. Together, these two studies illuminate distinct yet complementary pathways—one operating through immune activation and the other through metabolic reprogramming—that govern cancer dissemination and offer potential therapeutic targets.
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