由P-gp驱动的抗癌药物耐药性:生物特征,非编码RNA,药物和纳米调制剂
Yang Guo1, Milad Ashrafizadeh2, Murtaza M Tambuwala3
1Department of Respiratory and Critical Care Medicine, Shenyang Tenth People's Hospital (Shenyang Chest Hospital), No. 11 Beihai Street, Dadong District, Shenyang 110044, Liaoning, China.
癌症中耐药性通常是由P-glycoprotein (P-gp) 流动引起的. 这篇评论探讨了P-gpp之间的关系.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 药物耐药性显著降低了化疗的有效性.
- 通过P-glycoprotein (P-gp) 介导的药物外流是抵抗的一个关键机制.
- 了解P-gp的作用对于改善癌症治疗结果至关重要.
研究的目的:
- 审查P-gp在癌症抗药性中的作用.
- 阐明影响P-gp活性的分子途径和因素.
- 讨论克服P-gp介导抗性的潜在策略.
主要方法:
- 对P-gp和癌症抗药性研究的文献综述.
- 对包括PI3K-Akt,PTEN和NF-κB在内的分子通路的分析.
- 检查非编码RNA (ncRNA) 和细胞外囊泡的作用.
- 研究影响P-gp的代谢和能量依赖机制.
- 对P-gp抑制剂,如植物化学物质,小分子和纳米颗粒的调查.
主要成果:
- 在癌症中,P-gp失调显著导致多药性耐药性.
- 关键的分子通路 (PI3K-Akt,PTEN,NF-κB) 和ncRNAs调节了P-gp的功能.
- 细胞外囊泡在细胞间通信中发挥作用,影响P-gp活性.
- 通过线粒体功能障碍或抑制谷氨胺代谢来准依赖ATP的P-gp功能,可以增强化学敏感性.
- 各种P-gp抑制剂在恢复药物敏感性方面表现有前途.
结论:
- P-gp是克服化疗耐药性的关键目标.
- 通过各种分子和代谢策略调节P-gp活性,可以使癌细胞对药物重新敏感.
- 包括植物化学品和纳米粒子在内的P-gp抑制剂具有治疗潜力.
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