一种新型光敏感剂介导的光动力学疗法的抗瘤效应及其对细胞转录组的影响
Jingjing Chen1, Dan Wang2, Zequn Wang2
1Department of Pharmacology, School of Pharmacy, Changzhi Medical College, Changzhi, China.
Oncology research
|April 30, 2024
概括
这项研究表明,使用新型光敏感剂 (DTP) 的光动力疗法 (PDT) 能够有效抑制癌细胞生长. 通过活性氧物种 (ROS) 和亡,DTP-PDT诱导细胞死亡,涉及P38 MAPK通路并影响细胞周期基因.
科学领域:
- 在瘤学瘤学.
- 生物化学 生化学
- 分子生物学分子生物学
背景情况:
- 光动力疗法 (PDT) 是一种新兴的癌症治疗方式.
- 新型光敏感剂对于提高PDT疗效至关重要.
- 了解PDT的分子机制对于其临床应用至关重要.
研究的目的:
- 为了研究一种新型光敏感剂的抗瘤作用,即meso-5-[ρ-diethylene triamine pentaacetic acid-aminophenyl]-10,15,20-triphenyl-porphyrin (DTP),介导光动力学疗法 (DTP-PDT).
- 阐明DTP-PDT的潜在机制,包括其对细胞活力,活性氧物种 (ROS) 生成,亡,自和基因表达的影响.
主要方法:
- 细胞活力通过细胞计数工具-8测定来评估.
- 使用DCFH-DA光探头测量了ROS生成.
- 通过 Hoechst 染色和西部涂抹来评估亡与亡相关的蛋白质 (Bax, Bcl-2).
- 通过评估LC3B-II水平来监测自.
- 进行RNA测序和随后的生物信息分析 (GO,KEGG,疾病本体学,Reactome,PPI) 以确定差异表达的基因和途径.
主要成果:
- 在MCF-7和SGC7901癌细胞系中,DTP-PDT显著抑制细胞生长并诱导ROS生成.
- DTP-PDT诱导的细胞毒性被ROS清除剂 (NAC) 和P38 MAPK抑制剂 (SB203580) 减弱.
- 亡是由DTP-PDT诱导的,由改变的Bax/Bcl-2比率证明,这种效应也对NAC和SB203580敏感.
- DTP-PDT增加了LC3B-II的水平,表明诱导了自.
- RNA测序确定了3496个差异表达的mRNAs,富含与细胞周期,核糖体,DNA复制和蛋白质结合相关的途径,其中cdk1和rps27a被确定为关键相互作用基因.
结论:
- DTP-PDT通过抑制细胞增殖和诱导细胞亡和自,显示出显著的抗瘤活性.
- 这些机制涉及ROS生成和P38 MAPK信号通路的激活.
- 由DTP-PDT诱导的关键分子变化与细胞周期调节,核糖体功能,DNA复制和蛋白质结合有关,提供潜在的治疗点.
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