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C1Q⁺ TPP1⁺巨细胞通过SETD8驱动的p53甲基化促进结肠癌的进展

Veronica Veschi^1,2, Francesco Verona³, Sebastiano Di Bella⁴

¹Department of Precision Medicine in Medical, Surgical and Critical Care, University of Palermo, Palermo, 90127, Italy. veronica.veschi@uniroma1.it.

Molecular cancer

|April 1, 2025

概括

瘤抑制剂p53 (p53^K382me1) 的SETD8失活在结直肠癌 (CRC) 的发展中至关重要. 针对SETD8为晚期CRC提供了一个有前途的治疗策略,特别是在炎症引起的病例中.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

瘤抑制剂TP53在瘤中经常被功能性失活,但机制尚不清楚.
SETD8是唯一一种已知的酶,它在lysine 382 (p53^K382me1) 上单甲基化p53,抑制其瘤抑制功能.

研究的目的:

研究SETD8-介导的p53失活在结直肠癌 (CRC) 和炎症性肠病 (IBD) 中的作用.
评估p53^K382me1作为CRC的潜在生物标志物和治疗标.

主要方法:

在临床CRC和IBD样本中分析SETD8和p53^K382me1表达.
在CRC患者中整合大批和单细胞RNA测序 (RNAseq).
使用了组织病理学,ChIP测定和临床前体内CRC模型.

主要成果:

在CRC患者中,SETD8介导的p53调节是最显著丰富的途径.
p53^K382me1在结直肠癌干细胞 (CR-CSC) 和瘤相关巨细胞 (TAM) 中被发现,与生存率下降相关.
TAMs通过IL-6/MCP-1促进CR-CSC中的p53无活化,增强SETD8转录;SETD8抑制减少了瘤生长和转移.

结论:

p53^K382me1可能代表瘤发作的早期事件,特别是与炎症相关的CRC.
p53^K382me1显示出作为晚期CRC的预后生物标志物和治疗点的潜力.

关键词:

C1Q+ TPP1+ 大细胞在CRC中,CRC就是CRC.癌症干细胞是癌症干细胞.IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD IBD P53K382me1me1me1me1me1me1me1me1me1me1me1me3me3me3me3me3me3me3me3me3me3me3me3me3me3me3me3me3me3me 在SETD8中,它是SETD8.

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