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<p>Extravasation, the exit of cells from blood vessels, is essential in both development and disease, from germ cell migration to cancer metastasis. We show that all extravasating cells examined, avian primordial germ cells and diverse human cancer lines, form Ca²⁺-dependent membrane blebs during transendothelial migration. Yet the source of Ca²⁺ diverges by lineage. PGCs and HT-1080 fibrosarcoma cells rely on store-operated Ca²⁺ entry (SOCE), whereas epithelial-derived cancer cells such as PC-3 and MDA-MB-231 use IP₃R-mediated Ca²⁺ release from the endoplasmic reticulum. These findings establish bleb-based extravasation as a conserved morphodynamic strategy powered by distinct regulatory modules. Evolutionarily, they map onto an ancestral ER-release pathway and a metazoan-derived SOCE pathway. Conceptually, cancer blebbing emerges as a composite strategy that reactivates both ancient survival programs and developmental toolkits to maximize invasive success. This unified framework highlights Ca²⁺ supply as a critical bottleneck of vascular escape, offering new angles for targeting metastatic dissemination.</p>

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Bleb-based extravasation uses conserved morphodynamics but divergent calcium control

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月26日

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  • Mizuki Morita,
  • Manami Morimoto,
  • Junichi Ikenouchi,
  • Bertrand Pain,
  • Yuji Atsuta,
  • Yoshiki Hayashi,
  • Takayuki Teramoto,
  • Daisuke Saito

摘要

Extravasation, the exit of cells from blood vessels, is essential in both development and disease, from germ cell migration to cancer metastasis. We show that all extravasating cells examined, avian primordial germ cells and diverse human cancer lines, form Ca²⁺-dependent membrane blebs during transendothelial migration. Yet the source of Ca²⁺ diverges by lineage. PGCs and HT-1080 fibrosarcoma cells rely on store-operated Ca²⁺ entry (SOCE), whereas epithelial-derived cancer cells such as PC-3 and MDA-MB-231 use IP₃R-mediated Ca²⁺ release from the endoplasmic reticulum. These findings establish bleb-based extravasation as a conserved morphodynamic strategy powered by distinct regulatory modules. Evolutionarily, they map onto an ancestral ER-release pathway and a metazoan-derived SOCE pathway. Conceptually, cancer blebbing emerges as a composite strategy that reactivates both ancient survival programs and developmental toolkits to maximize invasive success. This unified framework highlights Ca²⁺ supply as a critical bottleneck of vascular escape, offering new angles for targeting metastatic dissemination.