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GBP2和M2巨细胞之间的交叉声会促进ccRCC的进展

Wei Zheng^1,2, Shujiang Ye^1,2, Bin Liu^1,2

¹Department of Urology, The First Affiliated Hospital of Anhui Medical University, Hefei, China.

|September 2, 2024

概括

关酸盐结合蛋白2 (GBP2) 通过与M2巨细胞相互作用,促进清细胞细胞癌 (ccRCC) 转移. 抑制GBP2可能为ccRCC提供新的治疗策略.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
癌症生物学癌症生物学

背景情况:

清细胞细胞癌 (ccRCC) 是一种具有高转移潜力的侵袭性癌.
酸结合蛋白2 (GBP2) 在ccRCC进展中的作用及其与瘤免疫的关系尚不清楚.

研究的目的:

研究GBP2在ccRCC转移中的功能作用.
阐明涉及M2巨细胞和关键信号通路的潜在机制.

主要方法:

在ccRCC中,GBP2表达和M2巨细胞之间的相关性分析.
在体外实验中评估ccRCC细胞迁移和在GBP2抑制时的入侵.
研究巨受条件介质对ccRCC细胞的影响.
对细胞因子分泌 (IL-10,TGF-β,IL-18) 和信号通路激活 (p-STAT3,p-ERK) 的分析.

主要成果:

GBP2表达与ccRCC中M2巨细胞的存在有很强的相关性.
GBP2抑制显著减少了ccRCC细胞迁移和入侵.
M2巨细胞可以逆转GBP2对ccRCC细胞运动的抑制作用.
M2巨细胞通过IL-10和TGF-β介导的GBP2/p-STAT3/p-ERK轴增强ccRCC细胞的入侵.
GBP2通过IL-18分泌促进M2巨细胞的两极分化.

结论:

GBP2通过调节瘤免疫力和巨细胞极化,在ccRCC转移中发挥着关键作用.
一个涉及GBP2,IL-18,M2巨细胞,IL-10,TGF-β,p-STAT3和p-ERK的反循环驱动了ccRCC的进展.
向GBP2为对抗ccRCC转移提供了一个潜在的治疗策略.

关键词:

2英2英2英2英2英一个IL-10的IL-10.一个IL-18,一个IL-18.在M2巨细胞中.在TGF-ββ.ccRCC ccRCC 在线观看转移转移转移转移

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