与肥胖相关的内质网膜应激对癌症和相关分子标的影响
Joud AlBashtawi1, Hend Al-Jaber2, Sara Ahmed2
1College of Medicine, QU Health, Qatar University, Doha P.O. Box 2713, Qatar.
Biomedicines
|April 27, 2024
概括
肥胖引起的内质网膜 (ER) 压力促进胰岛素抵抗和癌症. 针对ER压力路径,为与肥胖相关的疾病,包括癌症提供了新的治疗策略.
科学领域:
- 代谢障碍 代谢障碍 代谢障碍
- 在瘤学瘤学.
- 细胞应激生物学 细胞应激生物学
背景情况:
- 肥胖与细胞内膜网膜 (ER) 的压力有关,有助于胰岛素抵抗,2型糖尿病和癌症.
- 炎症途径 (例如,c-Jun N-终端激酶/JNK) 会加剧胰岛素抵抗.
- ER压力通过诸如血管内皮生长因子 (VEGF) 和未折叠蛋白质反应 (UPR) 等因素影响瘤细胞的存活和生长.
研究的目的:
- 综合审查肥胖导致的ER压力与癌症发病/进展之间的联系.
- 探索瘤信号与肥胖症中ER压力路径之间的相互作用.
- 突出潜在的治疗策略来管理癌症中肥胖引起的ER压力.
主要方法:
- 文献综述侧重于肥胖,ER压力,胰岛素抵抗和癌症的交叉点.
- 信号通路的分析,包括JNK,VEGF,UPR,ER相关蛋白降解 (ERAD),自和表观遗传调节.
- 检查针对ER压力的治疗干预措施.
主要成果:
- 肥胖引起的ER压力是胰岛素抵抗和癌症发展的重要因素.
- 在ER压力的背景下,UPR途径在细胞存活和细胞亡中起着双重作用.
- 致癌途径和ER压力机制之间的相互作用在肥胖个体中至关重要.
结论:
- 通过治疗性干预 (小分子,批准的药物,基因疗法) 来缓解ER压力显示出治疗与肥胖有关的癌症的前景.
- 对UPR,ERAD,自和表观遗传调节的进一步研究可能会揭示新的治疗点和生物标志物.
- 针对ER压力路径为管理与肥胖相关的代谢和瘤疾病提供了一个有希望的途径.
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