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在胰腺管道腺癌中,在高LDHA活性下,M-MDSC中的UPAR表达

Chikanori Tsutsumi¹, Kenoki Ohuchida^2,3, Kiwa Son¹

¹Department of Surgery and Oncology, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Fukuoka, 812-8582, Japan.

Scientific reports

|November 30, 2025

概括

胰腺癌中的高乳酸脱酶A (LDHA) 通过促进髓质衍生抑制细胞 (MDSCs) 来促进免疫抑制瘤微环境 (TME). 减少LDHA降低MDSC和胆固醇代谢,提供潜在的治疗点.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
代谢途径代谢途径

背景情况:

胰腺管道腺癌 (PDAC) 呈现出免疫抑制性瘤微环境 (TME),阻碍了治疗的有效性.
由乳酸脱酶A (LDHA) 生成的乳酸盐与TME免疫抑制有关,但其在PDAC中在代谢压力下免疫细胞调节中的确切作用尚不清楚.

研究的目的:

阐明高LDHA TME在PDAC中促进免疫抑制的机制.
研究乳酸代谢对PDAC内的免疫细胞群的影响.

主要方法:

使用了一个鼠标Ldha-knockdown (shLdha) PDAC模型.
采用单细胞RNA测序和多重免疫光染色.
分析了基因组的丰富性,重点关注胆固醇代谢和骨髓衍生抑制细胞 (MDSC) 中的PLAUR表达.

主要成果:

在PDAC模型中减少的LDHA导致MDSCs显著下降.
来自shLdha组的MDSC显示胆固醇代谢途径的丰富性降低.
编码尿素酶等离子体激活体受体 (uPAR) 的PLAUR在MDSC中表达很高,特别是单细胞MDSC (M-MDSC).
人类PDAC样本的高LDHA表达与M-MDSCs的增加和M-MDSCs上更高的UPAR表达相关.

结论:

由高LDHA驱动的乳酸代谢通过促进免疫抑制MDSCs显著影响PDAC TME.
这项研究确定了LDHA,胆固醇代谢,UPAR表达和PDAC中M-MDSC积累之间的联系.
这些发现为PDAC免疫抑制提供了机制性的见解,并建议针对LDHA-乳酸盐-MDSC轴的潜在治疗策略.

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