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代谢异质性导致黑色素瘤转移潜力的差异

Alpaslan Tasdogan¹, Brandon Faubert¹, Vijayashree Ramesh¹

¹Children's Research Institute and Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.

|December 20, 2019

概括

转移性黑色素瘤细胞依赖单碳酸盐载体1 (MCT1) 来控制氧化应激并促进转移. 通过破坏乳酸吸收和增加活性氧物种,抑制MCT1可降低转移负担.

科学领域:

癌症学
癌症新陈代谢
分子生物学

背景情况:

转移涉及癌细胞中复杂的代谢适应,尚未完全理解.
瘤内的代谢异质性可以影响转移潜力.

研究的目的:

研究新陈代谢差异,特别是单碳酸盐运输体1 (MCT1) 在黑色素瘤细胞转移中的作用.
确定MCT1功能如何影响营养处理,氧化应激和转移性传播.

主要方法:

在患者衍生的异种移植中进行同位素追踪.
药理上抑制MCT1.
营养吸收,氧化应激标志物 (活性氧物种) 和转移负担的分析.
高MCT1和低MCT1的黑色素瘤细胞群的比较.

主要成果:

有效转移的黑色素瘤表现出更高的MCT1水平,并且更明显地利用循环中的乳酸.
抑制MCT1降低了瘤的乳酸吸收,抑制了氧化酸盐通路,增加了活性氧物种.
在体内,MCT1抑制显著降低了循环瘤细胞和转移负担,对主要瘤生长的影响最小.
在静脉注射后,高MCT1细胞的转移潜力大于低MCT1细胞.

结论:

由MCT1介导的代谢差异是黑色素瘤转移潜力的关键决定因素.
对于转移黑色素瘤细胞来说,MCT1对于控制氧化应激和生存至关重要.
向MCT1是一种潜在的治疗策略,可以抑制黑色素瘤转移.

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