下一个细胞假设:与肥胖相关的致癌机制
Ayse Basak Engin1, Atilla Engin2,3
1Faculty of Pharmacy, Department of Toxicology, Gazi University, Hipodrom, Ankara, Turkey. abengin@gmail.com.
Advances in experimental medicine and biology
|September 17, 2024
概括
肥胖会增加癌症的风险和死亡率. 脂肪细胞衍生的外基因组调解细胞间通信,通过微RNA和其他分子影响瘤发育和转移.
科学领域:
- 在瘤学瘤学.
- 代谢疾病 代谢疾病
- 细胞生物学 细胞生物学
背景情况:
- 肥胖与增加的死亡率和癌症风险有关,表观遗传因素在倾向中发挥作用.
- 慢性炎症和癌症相关脂肪细胞 (CAAs) 在肥胖中促进瘤发育和转移.
- 脂肪组织释放出外体微RNA (miRNA),影响代谢途径和疾病并发症.
研究的目的:
- 探索通过外体细胞间通信在与肥胖相关的癌症发展中的作用.
- 讨论脂肪细胞与瘤细胞相互作用的机制,包括外体miRNA和"下一个细胞假设".
- 为了检查缺氧和Notch-interleukin-1 (IL-1) -Leptin交叉 (NILCO效应) 对与肥胖有关的癌症的影响.
主要方法:
- 关于肥胖,癌症,表观遗传学,外体和细胞通信的文献综述.
- 对外体miRNAs在调解代谢反应和癌症进展中的作用的分析.
- 讨论脂肪组织和瘤之间的共同致病特征,包括缺氧.
主要成果:
- 脂肪细胞衍生的外体作为信使,转移分子,改变细胞表型,促进瘤生长.
- 外基因组通过"下一个细胞假设"和脂肪细胞和瘤细胞之间的相互miRNA交换促进器官特异性转移.
- 肥胖和瘤的缺氧会加剧疾病,导致脂肪细胞功能障碍和癌症预后较差.
结论:
- 通过外体的细胞间通信,特别是脂肪细胞衍生的外体miRNA,对于与肥胖相关的癌症发展至关重要.
- "下一个细胞假设"和"尼尔科效应"为理解这些复杂的相互作用提供了框架.
- 向外体介导的通讯途径有可能成为针对肥胖相关癌症的新疗法策略.
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