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  3. 研究领域
  5. 生物医学和临床科学
  7. 瘤学和致癌症
  9. 预测和预后标志物
  11. 与肝脏再生相关的肝细胞yap1激活通过谷氨酸竞争防止结直肠癌肝脏转移

与肝脏再生相关的肝细胞YAP1激活通过谷氨酸竞争防止结直肠癌肝脏转移

Qiang Yu1, Mincheng Yu1, Peiyi Xie1

  • 1Department of Hepatobiliary Surgery and Liver Transplantation, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Shanghai 200032, P.R. China.

Science advances
|August 22, 2025

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在PubMed 上查看摘要

概括
此摘要是机器生成的。

大型肝切除术通过激活肝细胞YAP1信号来改善结直肠癌肝转移的存活率. 这一过程通过减少骨髓衍生抑制细胞透来增强抗瘤免疫力.

科学领域:

  • 肝胆外科手术
  • 癌症转移
  • 免疫学

背景情况:

  • 在肝切除术后,肝细胞与Yes相关的蛋白1 (YAP1) 信号被激活,可能抑制肝脏瘤.
  • 结肠直肠癌肝脏转移 (CRLM) 是一个重要的临床挑战.
  • 了解肝切除术对CRLM影响的机制至关重要.

研究的目的:

  • 为了比较CRLM患者的预后进行重大和轻微的肝切除术.
  • 阐明肝切除术影响CRLM生长和患者存活的分子机制.
  • 调查YAP1信号传递和对肝切除术反应的代谢变化.

主要方法:

  • 对240名接受肝切除术的CRLM患者进行了回顾性分析.
  • 通过注射MC38细胞诱导的CRLM的小鼠模型.
  • 对YAP1激活,表皮生长因子受体调节,胺代谢和免疫细胞透的分析.

主要成果:

  • 与轻微肝切除相比,CRLM患者和小鼠的肝切除与显著更好的生存相关.
  • 广泛的肝切除激活了肝细胞YAP1,改变了谷氨酸代谢,并增加了肝脏谷氨酸消耗.
  • 这导致瘤细胞缺乏谷氨酸,减少了YAP1活性,抑制了CXCL5的产生,减少了骨髓系抑制细胞的透,增强了CD8+ T细胞的功能.

结论:

  • 大型肝切除术通过激活肝细胞YAP1信号和重编程瘤微环境,为CRLM提供了生存益处.
  • 这种机制涉及代谢变化导致谷氨酸稀缺,瘤细胞YAP1活动减少,随后免疫调节.
  • 这些发现强调了YAP1和谷氨酸代谢作为CRLM的潜在治疗点.

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