在食道状细胞癌的进展中,circPDE3B和ferroptosis之间发现了一种新的联系
Pengli Zhou1, Zhengyang Wu1, Qinghui Zhang1
1Intervention Department, the First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan Province, PR China.
Genomics
|December 13, 2023
概括
循环PDE3B (circPDE3B) 通过抑制铁亡,促进食道状细胞癌 (ESCC). 它通过HNRNPK和miR-516b-5p分别准SLC7A11和CBS,推动瘤的生长.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 细胞死亡机制 细胞死亡机制
背景情况:
- 食道状细胞癌 (ESCC) 是一个重要的全球健康问题.
- 铁死是一种受调节的细胞死亡形式,与癌症的进展有关.
- 循环RNAs (circRNAs) 在ESCC和ferroptosis中的作用仍然不完全理解.
研究的目的:
- 研究circPDE3B在ESCC进展中的作用.
- 阐明circPDE3B通过哪些机制影响ESCC中的铁亡.
- 探索ESCC中circPDE3B通路的潜在治疗向.
主要方法:
- 对人类ESCC组织和细胞系进行分析,以评估铁亡标记物 (铁,ROS,GSH,MDA).
- 流细胞计用于细胞亡和细胞循环分析.
- 分子测试包括FISH,RNA拉下,RIP和光酶测试,以确定分子相互作用.
- 在体内验证使用裸体老鼠异种移植模型.
主要成果:
- 在ESCC组织中增加circPDE3B水平与SLC7A11和CBS表达相关.
- 在ESCC细胞中抑制circPDE3B诱导的铁亡,细胞亡和细胞循环停止.
- circPDE3B 作为 miR-516b-5p 的海绵,上调 CBS,并与 HNRNPK 结合稳定 SLC7A11,从而抑制铁亡并促进 ESCC 的生长.
结论:
- 通过抑制铁亡,circPDE3B促进ESCC的进展.
- 这些circPDE3B/HNRNPK/SLC7A11和circPDE3B/miR-516b-5p/CBS轴是驱动ESCC的关键机制.
- 向circPDE3B可能代表ESCC的新疗法策略.
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