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PANoptosis的表观遗传调节:DNA甲基化,基因素修饰和非编码RNAs
Yogendra Singh1, Muhammad Afzal2, M Arockia Babu3
1Department of Pharmacology, Maharishi Arvind College of Pharmacy, Ambabari, Jaipur, Rajasthan, India.
EXCLI journal
|March 16, 2026
概括
编程细胞死亡 (PANoptosis) 的表观遗传调节是癌症治疗的关键. 基因甲基化和基因素修饰控制了PANoptosis的敏感性,为克服抗化学性提供了新的目标.
科学领域:
- 细胞生物学 细胞生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 癌症治疗 癌症治疗
背景情况:
- 编程的细胞死亡途径,包括亡,烧亡和亡,汇聚在PANoptosomes中.
- PANoptotic传感器,适配器和效应器的表观遗传调节对于细胞反应和癌症治疗至关重要.
- 瘤中PANoptosis的失调有助于瘤中的化学抵抗.
研究的目的:
- 阐明控制PANoptosis的表观遗传机制.
- 探索表观遗传修饰在调节PANoptotic敏感性和化学抵抗中的作用.
- 为了确定癌症治疗的潜在表观遗传治疗策略.
主要方法:
- 对影响关键PANoptotic基因 (RIPK3,GSDME,CASP8) 的DNA甲基化模式的分析.
- 通过BRD4/p300调解的组蛋白修饰 (H3K27ac) 的研究及其对基因转录的影响.
- 对调节PANoptotic基因可访问性的染色体重塑复合体 (SWI/SNF,NuRD) 的评估.
- 在转录后调节中检查像miR-223-3p和lncRNA NEAT1这样的非编码RNA (ncRNA).
主要成果:
- DNA甲基化抑制了PANoptotic通路,导致化学抵抗;低甲基化恢复了敏感性.
- 通过BRD4/p300进行的素乙化增强了ZBP1,NLRP3和caspase-8的转录,而HDAC则抑制了炎症体的形成.
- 染色体重塑剂SWI/SNF和NuRD动态调节PANoptotic区域的可访问性.
- ncRNAs汇聚以调节NLRP3,RIPK3和GSDMD的表达,影响PANoptotic的敏感性.
- 表观遗传相互作用创造了决定PANoptotic敏感性的值.
结论:
- 表观遗传修饰,包括DNA甲基化,基因素乙化和ncRNAs,是PANoptosis的关键调节者.
- 向表观遗传通路提供了一个有希望的策略,以克服瘤化学抵抗.
- 与DNMT抑制剂,HDAC调节剂和PANoptosis激动剂的联合治疗可以提高癌症治疗的疗效并降低毒性.
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