帕丘利酒精诱导G0 /G1细胞循环停止和亡在温克里斯耐药的非小细胞肺癌通过ROS介导的DNA损伤
Chi-Yen Liang1, Kai-Fu Chang2, Ya-Chih Huang2,3
1Division of Pulmonary Medicine, Department of Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi, Taiwan, ROC.
Thoracic cancer
|May 30, 2023
概括
帕丘利酒精 (PA) 通过诱导DNA损伤和亡来治疗非小细胞肺癌 (NSCLC) 是有前途的. 它还可以克服耐药性,并增强西斯的作用.
科学领域:
- 分子生物学分子生物学
- 癌症研究 癌症研究
- 药理学 药理学是指药理学的学科.
背景情况:
- 非小细胞肺癌 (NSCLC) 是全球癌症死亡的主要原因.
- 芬克里斯 (VCR) 用于NSCLC,但由于副作用和耐药性而面临限制.
- 帕丘利酒精 (PA) 来自Pogostemon cablin,表现出已知的抗炎和抗癌特性.
研究的目的:
- 调查帕丘利酒精 (PA) 在诱导反应性氧物种 (ROS) 介导的DNA损伤中的作用.
- 评估PA对NSCLC细胞系的影响,包括对VCR抗性变异.
- 探索PA作为NSCLC治疗剂的潜力.
主要方法:
- 通过MTT试验,殖民地形成试验和流细胞计评估抗癌潜力.
- 通过使用西部涂抹,DCFDA染色,免疫光和TUNEL测定来研究机制.
- 分析了耐药性和癌症干细胞标记物.
主要成果:
- 治疗PA增加了细胞内ROS水平,激活CHK1/CHK2信号通路.
- PA抑制了增殖,诱导了G0/G1细胞周期停止,并通过内在途径促进了细胞亡.
- 低调PA药物耐药性 (p-糖蛋白) 和癌症干细胞标记物 (CD44,CD133);观察到与西斯的协同效应.
结论:
- 帕丘利酒精诱导ROS介导的DNA损伤,细胞循环停止和NSCLC细胞的亡.
- 它可以减弱药物耐药性和癌症干细胞表型.
- 帕显示了NSCLC治疗的潜力,特别是在与西斯普拉丁结合时,即使在VCR耐药的情况下也是如此.
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