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在食道状细胞癌中,PTGDS缺乏作为M2巨分化和免疫抑制微环境的驱动因素:一项实验性研究

Jian Zhong¹, Yujie Xie², Zhengang Zhao¹

¹Department of Thoracic Surgery, Affiliated Gaozhou People's Hospital of Guangdong Medical University, Guangdong, China.

International journal of surgery (London, England)

|June 11, 2025

概括

前列腺素D2合成酶 (PTGDS) 缺乏在食道状细胞癌 (ESCC) 中促进免疫抑制性瘤微环境 (TME),导致生存率低下. 对于ESCC患者来说,PTGDS可以作为预后生物标志物.

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:

食道状细胞癌 (ESCC) 与预后不佳有关,原因是M2巨极化瘤微环境 (TME).
质腺素D2合成酶 (PTGDS) 正在研究其在调节ESCC TME中的作用.

研究的目的:

阐明PTGDS在ESCC TME中的功能.
评估PTGDS在ESCC中的预后意义.

主要方法:

使用免疫解卷和WGCNA对转录基因数据集 (GSE53624,GSE121931) 的分析.
在高州队列中对差异表达基因和考克斯回归的评估.
使用免疫组织化学 (IHC) 开发和验证基于PTGDS的诺姆图.
在体外和体内实验来确认PTGDS功能.

主要成果:

在ESCC组织中,PTGDS显著下调,较低的表达与较差的整体存活率 (OS) 相相关.
一个基于PTGDS的名图显示了强大的预测准确性OS (1,3,5年AUCs:0.63,0.77,0.83).
较低的PTGDS表达与肌髓衍生抑制细胞增加,T细胞透减少和T细胞细胞毒性受损有关.
IHC证实PTGDS低瘤中M2巨细胞透率较高;PTGDS过度表达抑制了M2极化.

结论:

在ESCC中,PTGDS缺乏会促进免疫抑制性TME.
减少PTGDS表达预测不良的临床结果,并可能作为ESCC的预后生物标志物.

关键词:

食管状细胞癌的癌症巨细胞是一个巨细胞.两极分化是一种极化.瘤微环境是一个微环境.

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