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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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巨细胞的激活决定了胰腺癌中的肌肉消耗.

Chia-Jung Chang1, Po-Hsien Huang2,3, Szu-Ying Chen4

  • 1Department of Biomedical Engineering, National Cheng Kung University, Tainan, Taiwan.

Oncogene
|May 29, 2025
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概括

在携带瘤的小鼠中,卡切西亚的出现与特定的巨细胞信号有关,特别是CHI3L1.1. 用抗CHI3L1抗体向这种途径可以减少肌肉消耗,瘤生长和转移.

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科学领域:

  • 在瘤学瘤学.
  • 免疫学 免疫学 免疫学
  • 分子生物学分子生物学

背景情况:

  • 瘤微环境中的非癌细胞对缓解症的贡献仍然不太清楚.
  • 卡赫克西亚发病的精确时间和细胞起源是不可预测的,尽管癌症卡赫克西亚研究取得了进展.

研究的目的:

  • 为了研究瘤微环境中的非癌细胞在驱动缓存症中的作用.
  • 在胰腺癌模型中识别特定的细胞类型和负责早期肌肉衰竭的分子信号.
  • 为了阐明 cachexia 进展中的 CHI3L1-HDAC3 信号轴.

主要方法:

  • 使用了一种转基因的KrasLSL-G12D/+;Trp53flox/flox;Pdx1-Cre (KP2C) GEMM用于胰腺癌.
  • 在外周血液单核细胞 (PBMC) 和来自小鼠的同源移植 (MDST) 上进行单细胞RNA测序 (scRNA-seq).
  • 研究了CHI3L1对C2C12髓母细胞的影响,并使用了骨肌特异性的条件Hdac3淘汰赛小鼠.

主要成果:

  • scRNA-seq确定了CHI3L1和CHI3L3作为差异表达的基因,其中巨细胞调解了早期的肌肉衰竭.
  • 重组CHI3L1抑制了髓管的形成,并提高了神经细胞中的特定炎症和信号基因的调节.
  • 通过Hdac3淘汰赛或抗CHI3L1抗体治疗准CHI3L1-HDAC3信号,可以减少肌肉消耗,瘤生长和转移.

结论:

  • 胰腺瘤相关的巨细胞在调解骨肌肉消耗方面发挥着重要作用.
  • CHI3L1-HDAC3信号通路是驱动缓冲症进展的关键机制.
  • 向CHI3L1提供了一种潜在的治疗策略,以对抗癌症缓解症和相关的瘤进展.