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探索黑色素瘤特异性Bcl-xL与瘤免疫微环境的关联

Anna Maria Lucianò^1,2,3,4, Marta Di Martile⁵, Ana B Pérez-Oliva³

¹Preclinical Models and New Therapeutic Agents Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.

Journal of experimental & clinical cancer research : CR

|July 24, 2023

概括

黑色素瘤细胞中的Bcl-xL蛋白过度表达通过招募巨细胞并诱导由特定的细胞因子和NF-kB信号调节的瘤前驱M2表型,促进瘤进展.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

巨细胞是瘤微环境的关键组成部分,有可能采用瘤相关巨细胞 (TAM) 现型.
TAMs可以促进瘤的进展,并影响治疗反应.
Bcl-2家族成员Bcl-xL在黑色素瘤中受到放松,并影响瘤进展,而不仅仅是其抗亡作用.

研究的目的:

研究Bcl-xL在黑色素瘤中巨细胞招募和极化中的作用.
为了确定特定的细胞因子和参与Bcl-xL介导的巨细胞调节的信号通路.

主要方法:

使用了具有改变Bcl-xL表达的人类黑色素瘤细胞,THP-1单细胞细胞和单细胞衍生的巨细胞.
采用蛋白质阵列,中和抗体,qRT-PCR,ELISA,Western Blot和Transwell迁移分析.
在人类和斑马鱼黑色素瘤模型中验证的结果.

主要成果:

过度表达Bcl-xL的黑色素瘤细胞招募了巨细胞,并诱导了M2极化表型.
鉴定了介质素-8和介质素-1β作为巨分极的关键细胞因子.
鉴定出CCL5/RANTES是负责巨细胞招募的化学激素.
这些Bcl-xL诱导的效应被证明是NF-kB依赖的.

结论:

Bcl-xL通过调节巨细胞表型,在黑色素瘤中起到促瘤作用.
准Bcl-xL或其下游信号可能为黑色素瘤提供治疗策略.

关键词:

在 Bcl-xL 中.黑色素瘤是一种黑色素瘤.与瘤相关的巨细胞.

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