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<p>Extracellular vesicles (EVs) play a vital role in ovarian carcinoma (OvCa) metastasis, yet the mechanisms regulating EV biogenesis remain unclear. Here, we identify CBX2 as a key driver of omental metastasis, with elevated expression in metastatic lesions and association with poor prognosis. CBX2 promotes tumor cell migration, invasion, and metastasis by enhancing EV secretion and pro-metastatic cargo loading through remodeling lipid rafts, cholesterol-rich membrane microdomains essential for EV formation. Deletion of the intrinsically disordered region abolishes lipid raft remodeling and multivesicular body redistribution, indicating dependence on liquid-liquid phase separation (LLPS). CBX2 also transcriptionally upregulates FLOT1 in an LLPS-dependent manner. Disruption of lipid rafts or inhibition of CBX2 phase separation markedly reduces EV production and metastatic potential. These findings reveal an LLPS-dependent mechanism linking CBX2 to lipid raft-mediated EV biogenesis and OvCa metastasis.</p><p></p>

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Liquid-liquid phase separation of CBX2 regulates lipid raft-mediated extracellular vesicle biogenesis to facilitate ovarian carcinoma metastasis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月4日

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  • Qiulei Wu,
  • Xiaohan Xu,
  • Xiaoli Liu,
  • Wenhan Li,
  • Guoqing Li,
  • Lanqing Gong,
  • Lin Huang,
  • Pan Liu,
  • Feiquan Ying,
  • Tong Liu,
  • Yuanyuan Li,
  • Wenting Zhang,
  • Xinyi Wu,
  • Yisu Gao,
  • Si Sun,
  • Zehua Wang,
  • Jing Cai,
  • Jianfeng Guo,
  • Lin Liu,
  • Ping Yang

摘要

Extracellular vesicles (EVs) play a vital role in ovarian carcinoma (OvCa) metastasis, yet the mechanisms regulating EV biogenesis remain unclear. Here, we identify CBX2 as a key driver of omental metastasis, with elevated expression in metastatic lesions and association with poor prognosis. CBX2 promotes tumor cell migration, invasion, and metastasis by enhancing EV secretion and pro-metastatic cargo loading through remodeling lipid rafts, cholesterol-rich membrane microdomains essential for EV formation. Deletion of the intrinsically disordered region abolishes lipid raft remodeling and multivesicular body redistribution, indicating dependence on liquid-liquid phase separation (LLPS). CBX2 also transcriptionally upregulates FLOT1 in an LLPS-dependent manner. Disruption of lipid rafts or inhibition of CBX2 phase separation markedly reduces EV production and metastatic potential. These findings reveal an LLPS-dependent mechanism linking CBX2 to lipid raft-mediated EV biogenesis and OvCa metastasis.