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在肺腺癌中,NFATc2通过USP17促进乳酸和M2巨的两极分化

Liang Wang¹, Yuanyuan Ma¹, Shanyuan Zhang¹

¹Department of Thoracic Surgery II, Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital and Institute, Beijing.

Anti-cancer drugs

|February 22, 2024

概括

激活T细胞c2的核因子 (NFATc2) 通过通过USP17调节增加乳酸盐水平和M2巨细胞极化来促进肺癌的进展.

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:

免疫细胞,特别是巨细胞,在瘤微环境中至关重要,并影响瘤的进展.
肺腺癌包括癌细胞和免疫透物之间的复杂相互作用.

研究的目的:

研究激活T细胞c2 (NFATc2) 的核因子在调节肺腺癌中的巨细胞特性中的作用.
阐明NFATc2影响肺腺癌进展的分子机制.

主要方法:

对肺腺癌组织与正常组织中的NFATc2表达的分析.
利用癌症基因组图谱 (TCGA) 数据集来确定NFATc2和缺氧/糖解相关基因之间的相关性.
采用单细胞测序数据来评估NFATc2与免疫细胞和巨细胞两极分化之间的关联.
研究了NFATc2对USP17基因促进者的转录调节.
评估了NFATc2抑制剂对乳酸盐水平和M2巨细胞极化的影响.

主要成果:

与正常肺组织相比,NFATc2表达在肺腺癌组织中显著更高.
NFATc2与参与肺腺癌缺氧和糖解的基因呈正相关性.
NFATc2与透免疫细胞有关,并影响了巨细胞的两极分化.
NFATc2直接与USP17促进体结合,增强肺腺癌细胞迁移和乳酸生产.
NFATc2还促进了巨细胞中的M2极化.
抑制NFATc2降低了乳酸盐水平和M2巨细胞极化.

结论:

在肺腺癌中,NFATc2作为关键调节剂.
NFATc2通过转录调节USP17.促进乳酸盐水平的增加和M2巨细胞的两极分化.
向NFATc2可能通过调节瘤微环境来为肺腺癌提供治疗策略.

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