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基因生成通过OTUD7Bβ-氧丁化激发了对恩扎拉胺耐药前列腺癌的免疫抑制
Haoran Jiang1, Yuan Zeng2, Weiqiang Ning3
1Department of Urology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China; Institute of Urology, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China; Zhejiang Key Laboratory of Critical Care Medicine,Wenzhou, 325000,Zhejiang China; Translational Medicine Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, Zhejiang, China; Key Laboratory of Novel Nuclide Technologies on Precision Diagnosis and Treatment & Clinical Transformation of Wenzhou City, Wenzhou, 325035, Zhejiang, China; Department of Radiation Oncology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
前列腺癌对恩扎胺的耐药性涉及到抑制免疫系统的代谢变化. 上调的基路径导致β-基酸盐的积累,导致免疫荒漠化和免疫疗法耐药性.
科学领域:
- 在瘤学瘤学.
- 代谢途径 代谢途径
- 免疫学 免疫学 免疫学
背景情况:
- 雄激素受体抑制剂是转移性前列腺癌的标准.
- 快速的耐药性发展限制了治疗的有效性.
- 恩扎胺耐药性与免疫抑制性瘤微环境有关.
研究的目的:
- 研究将恩扎拉胺耐药性与免疫逃脱联系在一起的机制.
- 确定驱动耐药性和免疫抑制的代谢适应.
- 探索潜在的治疗目标,以克服抵抗.
主要方法:
- 分析因子胺诱导的抵抗割的前列腺癌模型.
- 对基路酶表达的评估.
- 研究β-基酸盐 (BHB) 对蛋白质修饰的影响 (OTUD7B).
- 对cGAS-STING通路激活和干扰素表达的评估.
主要成果:
- 在抗性前列腺癌中明显过度表达基通路酶.
- 由于基路的上调,BHB的积累.
- 通过BHB介导的OTUD7B的β-hydroxybutyrylation损害了APC/C基质的降解.
- 细胞质dDNA减少,cGAS-STING激活减弱,干扰素表达减少.
结论:
- 通过基路的新陈代谢重编程有助于免疫荒漠化在酶胺耐药前列腺癌.
- 由BHB驱动的OTUD7B修改是免疫逃避的一个关键机制.
- 准代谢适应可能会提高前列腺癌免疫疗法的疗效.
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