在Cachectic Adipocytes中,STAT3信号驱动着LDH上调和平蛋白下调
Michele Mannelli1, Bianca Bartoloni1, Giulia Cantini1
1Dipartimento di Scienze Biomediche, Sperimentali e Cliniche "M. Serio", Università degli studi di Firenze, Viale Morgagni 50, 50134 Firenze, Italy.
International journal of molecular sciences
|November 25, 2023
概括
癌症相关的缓冲症涉及脂肪细胞的代谢变化,由瘤分泌体驱动. STAT3信号改变了乳酸脱酶和阿迪波内克丁,导致了这种衰弱的情况.
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:
- 卡切西亚显著损害了癌症患者的生活质量和治疗疗效.
- 了解脂肪细胞中缓存症的分子机制对于开发治疗策略至关重要.
研究的目的:
- 为了研究结肠癌秘对脂肪细胞代谢的影响.
- 为了确定参与脂肪细胞癌症诱导的缓解症的关键信号通路.
主要方法:
- 用CT26结肠癌细胞的分泌物治疗小鼠和人类脂肪细胞.
- 评估代谢变化,包括乳酸生产和氧气消耗.
- 通过牛酸盐抑制乳酸脱酶,并通过WP1066.6.使用STAT3信号进行抑制.
主要成果:
- 在脂肪细胞中,CT26分泌体诱导了卡塞克特特征,其特征是乳酸生产增加和氧气消耗减少.
- 氧沙治疗部分逆转了CT26分泌基因的代谢效应.
- 在STAT3信号通路的介导下,CT26分泌体增加了乳酸脱酶和减少了阿迪波内克丁的表达.
结论:
- STAT3信号级联是癌症相关缓解症期间脂肪细胞代谢变化的关键驱动因素.
- 准STAT3信号可能提供一种治疗方法,以减轻与缓解症相关的代谢功能障碍.
- 这些发现有助于在细胞和分子层面上更好地理解缓解症的病原性.
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