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来自易斯肺癌的外体EIF5A诱导脂肪细胞在癌症缓解症中消耗

Hairong Xiong¹, Jiaxin Ye², Qianqian Luo¹

¹Department of Pathogenic Biology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Cellular signalling

|September 24, 2023

概括

癌症缓解症涉及由炎症驱动的体重减轻. 这项研究发现,来自癌细胞的外体EIF5A诱导脂肪分解 (脂解),为缓解症治疗提供了潜在的新标.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
代谢过程中的代谢.

背景情况:

癌症缓解症是一种复杂的综合征,导致肌肉和脂肪消耗,导致生理衰退.
来自癌细胞的细胞外囊泡 (EV) 参与脂肪细胞脂解,但潜在的机制尚不清楚.

研究的目的:

为了调查来自易斯肺癌 (LLC) 细胞的EVs在癌症缓解症中的作用.
阐明癌细胞衍生的EVs在脂肪细胞中诱导脂解的机制.

主要方法:

来自LLC的电动汽车的提取和描述.
在体外研究中,使用3T3-L1和HIB1B脂肪细胞治疗LLC EVs.
在体内癌症缓解症小鼠模型.
西方斑点,甘释放和油红色O染色试验.
静止EIF5A并使用抑制剂GC7.

主要成果:

来自LLC的EV被脂肪细胞内部化,并通过外体EIF5A诱导脂解.
在EV中增加EIF5A表达与脂质代谢相关,肺癌患者的生存率较差.
抑制EIF5A在体外和体内减少脂肪细胞和脂肪组织脂解.
发现EIF5A可以结合GPBAR1mRNA,促进翻译和激活CREB通路以诱导脂解.

结论:

来自癌细胞的外体EIF5A促进癌症缓解症中的脂肪细胞脂解.
在EV中催眠的EIF5A在脂肪组织消耗中起着关键作用.
外体EIF5A代表了一种新的调节剂和癌症缓解症的潜在治疗标.

关键词:

脂肪细胞浪费的浪费癌症缓解症是一种癌症缓解症.单核细胞翻译启动因子5 A 细胞外囊泡中的细胞外囊泡.

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