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在初级固体瘤中缓慢的TCA流和ATP产生

Caroline R Bartman^1,2,3, Daniel R Weilandt^1,2,3, Yihui Shen^1,2

¹Department of Chemistry, Princeton University, Princeton, NJ, USA.

|February 1, 2023

概括

由于三碳酸 (TCA) 循环代谢被抑制,固体瘤的ATP产生速度比正常组织慢. 癌细胞通过减少能源密集型功能来适应持续生长.

科学领域:

生物化学
癌症生物学
代谢途径

背景情况:

组织通过糖解和三碳酸 (TCA) 循环产生ATP.
虽然TCA代谢在哺乳动物中占主导地位,但其在瘤中的速度尚不清楚.
沃伯格效应描述了癌细胞中糖分的增加.

研究的目的:

在各种小鼠组织和癌症模型中测量糖解和TCA循环的绝对速率.
根据测量的路径流量计算总ATP合成速率.
研究固体瘤,转移和白血病的代谢适应.

主要方法:

优化了用于代谢流量分析的标记剂输液技术.
在健康和癌症小鼠组织中量化糖解和TCA循环速率.
从路径流量数据计算净ATP合成速率.

主要成果:

在所有五种主要固体瘤模型中,TCA循环流被抑制.
在瘤中,糖解流量增加,但不足以抵消ATP生产的TCA流量减少.
固体瘤的ATP生成速度通常比健康组织慢.
与原发性乳腺癌相比,肺转移显示TCA流量增加.
胰腺癌通过降低蛋白质合成而适应,

结论:

固体瘤不是高代谢的;它们通常以较低的速度产生ATP.
尽管ATP的合成有限, 但癌细胞却需要耗费大量能量才能生长.
代谢重编程,包括抑制TCA循环和减少蛋白质合成,对于瘤的发展至关重要.

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