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SIRT6通过抑制TNFR2信号在小鼠中改善癌症和白内障相关的脂肪浪费

Kang Xu^1,2, Yida Wang¹, Fang Wang³

¹Protein Science Key Laboratory of the Ministry of Education, School of Pharmaceutical Sciences, Tsinghua University, Beijing, China.

Journal of cachexia, sarcopenia and muscle

|February 19, 2025

概括

赛尔图因6 (SIRT6) 通过抑制脂肪组织的消耗和脂解来保护癌症缓解症. 增加SIRT6水平或活性可能为这种衰弱的疾病提供一种新的治疗策略.

科学领域:

生物化学生化学
分子生物学分子生物学
在瘤学瘤学.

背景情况:

卡切西亚是一种与癌症相关的严重消耗综合征,其特点是代谢失衡和组织损失,导致发病率和死亡率增加.
目前治疗卡赫克西亚的治疗选择有限,缺乏临床验证.
作为能量恒温的关键调节剂,Sirtuin 6 (SIRT6) 正在研究其对抗癌症诱导的缓解症的保护作用.

研究的目的:

为了研究SIRT6对易斯肺癌 (LLC) 诱导的缓解症的保护作用.
评估血清SIRT6水平与患者癌症缓解症发展之间的相关性.
阐明SIRT6在卡赫克西亚期间对脂肪组织代谢的影响背后的机制.

主要方法:

在胃癌患者和健康对照人群中测量了血清SIRT6水平.
给SIRT6转基因 (TG) 和野生型 (WT) 的小鼠注射了LLC细胞以评估缓存症.
实验室研究探讨了SIRT6对脂肪细胞脂解的影响以及SIRT6激活剂 (MDL800) 的影响.

主要成果:

在非甲状腺癌患者中,SIRT6度高于甲状腺癌患者,这表明存在负相关性.
通过抑制棕色化和脂解,SIRT6过度表达显著降低了白色脂肪组织中瘤诱导的浪费和能量消耗.
瘤坏死因子-α受体2 (TNFR2) 介导着SIRT6抑制脂解信号传递;在缓解性患者中观察到血清TNFR2增加.
SIRT6激活剂MDL800逆转了脂肪细胞中LLC诱导的脂解.

结论:

SIRT6在减轻癌症缓解症方面发挥着有益作用.
增加SIRT6的表达或活性可以防止卡切西亚相关的组织损失.
调节SIRT6呈现出一种潜在的治疗策略,用于缓冲症.

关键词:

在SIRT6上这种SIRT6激活器是SIRT6激活器.这是一种TNFR2抗剂.脂肪的消耗是脂肪的消耗.卡赫西亚 (Cachexia) 是一种缓解症.

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