慢性压力通过CTCFF介导的circMBOAT2上调促进非小细胞肺癌 (NSCLC) 的进展
Ting Zhou1, Zhicong Chen2, Yitian Chen3
1Department of Pharmacy, Shanghai University of Medicine & Health Sciences Affiliated Sixth People's Hospital South Campus, Shanghai, China.
慢性压力通过circMBOAT2促进非小细胞肺癌 (NSCLC) 的进展,由CTCF调节. 沉默circMBOAT2或CTCF抑制瘤生长,为NSCLC和并发性抑郁症提供潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 压力生理学 压力生理学
背景情况:
- 循环RNAs (circRNAs) 越来越多地被认为是它们在癌症发展中的作用.
- 非小细胞肺癌 (NSCLC) 的进展是复杂的,并且可能受到慢性压力等外部因素的影响.
- 了解压力和癌症之间的分子机制对于有效的治疗策略至关重要.
研究的目的:
- 研究circMBOAT2在慢性压力条件下的NSCLC进展中的调节作用.
- 在压力诱导瘤发生的背景下,确定circMBOAT2的上游调节器.
- 探索circMBOAT2作为NSCLC和相关抑郁症的潜在治疗点.
主要方法:
- 构造的细胞系与circMBOAT2过度表达和淘汰.
- 进行了扩散,迁移和入侵分析 (殖民地形成,划伤愈合,Transwell,CCK-8).
- 建立了一个慢性不可预测的轻度压力 (CUMS) 鼠标模型,并利用CTCF敲击实验.
主要成果:
- 在NSCLC细胞和组织中,circMBOAT2被显著上调.
- circMBOAT2 降低抑制了 NSCLC 细胞的增殖,迁移和入侵;北上腺素逆转了这种效应.
- CUMS促进了瘤生长,而circMBOAT2沉默抑制了瘤生长.
- CTCF被确定为circMBOAT2的上游监管机构,其淘汰扭转了CUMS诱导的影响.
结论:
- 通过circMBOAT2.2,CTCF调解了慢性压力诱导的NSCLC的进展.
- circMBOAT2在NSCLC瘤发生中起着关键作用,特别是在慢性压力下.
- circMBOAT2代表了NSCLC和并发性抑郁症的潜在生物标志物和治疗标.
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