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全基因组体内查识别了转移殖民的新宿主调节剂

Louise van der Weyden¹, Mark J Arends², Andrew D Campbell³

¹Wellcome Trust Sanger Institute, Wellcome Genome Campus, Cambridge CB10 1SA, UK.

|January 5, 2017

概括

研究人员对810种突变小鼠进行了查, 寻找控制癌症转移的基因. 通过改变免疫细胞分布,删除斯芬戈-1-转运体Spns2显著降低了肺转移.

科学领域:

癌症学
免疫学
遗传学

背景情况:

癌症的转移是癌症相关死亡的主要原因.
瘤细胞殖民,而不是早期的转移,决定了转移性疾病的进展.
瘤微环境在调节转移殖民中起着至关重要的作用.

研究的目的:

使用大型体内遗传查,识别转移殖民的宿主微环境调节剂.
发现新基因与宿主控制癌症转移有关.

主要方法:

进行了810个突变小鼠线的前置遗传查,使用体内测试进行转移殖民.
在注射瘤细胞后,对野生类型和突变小鼠进行了肺转移焦点的定量分析.
研究了Sphingosine-1-phosphate (S1P) 信号通路和淋巴细胞的流通情况.

主要成果:

检测发现了23个调节瘤细胞殖民化的基因,其中19个基因以前与宿主控制转移无关.
缺少新娘同类物质2 (Spns2) 的小鼠表现出肺转移最显著的减少.
Spns2 缺乏导致循环淋巴缺血,肺部T细胞和自然杀手细胞的比例增加.

结论:

在调节宿主对转移性癌症的免疫反应方面,Spns2起着至关重要的作用.
通过 Spns2 删除改变淋巴细胞流通,增强肺部的抗瘤免疫力,减少转移负担.
这项研究确定了可以向控制癌症转移的新型宿主衍生因素.

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