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Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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双重敏感化使乳腺癌的协同光动力疗法和放射疗法成为可能.

Yingying Zhang1, Shaoqing Chen1, Chun Liu1

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概括

这项研究介绍了FCA,这是一种新的纳米平台,通过重塑瘤微环境和放大氧化应激来增强乳腺癌治疗. FCA-光动力疗法-放射疗法 (PDT-RT) 协同打击瘤,提供了一个有希望的剂量节约策略.

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科学领域:

  • 生物医学工程 生物医学工程
  • 纳米技术 纳米技术
  • 癌症治疗 癌症治疗

背景情况:

  • 使用放射疗法 (RT) 和光动力疗法 (PDT) 治疗乳腺癌,由于瘤缺氧和光敏剂效率低下而面临限制.
  • 开发先进的纳米平台对于克服这些挑战和改善治疗结果至关重要.

研究的目的:

  • 开发和评估一种新型的叶酸修饰铜碳点纳米平台 (FCA),载有5-氨基氨酸 (ALA),用于协同治疗乳腺癌.
  • 调查FCA重塑瘤微环境的能力,增强活性氧物种 (ROS) 生成,并使癌细胞对RT和PDT敏感.

主要方法:

  • 制造具有级纳米酶活动的FCA纳米平台,用于H2O2分解,ROS生成和谷氨酸 (GSH) 耗尽.
  • 评估FCA对ALA转化为原氨酸IX的影响以及随后的ROS放大.
  • 评估FCA-PDT-RT协同作用降低4T1乳腺癌细胞活力,诱导细胞亡,并触发细胞循环停止.
  • 对NRF2-KEAP1-HMOX1通路激活和代谢危机诱导的分析.
  • 在体内使用4T1乳腺癌模型进行体内研究,以评估瘤控制,免疫细胞透,血管生成和安全.

主要成果:

  • FCA有效地分解了H2O2,耗尽了GSH,并放大了ROS生成,启动了瘤微环境.
  • 与NRF2-KEAP1-HMOX1通路激活相关的FCA-PDT-RT显著降低了4T1细胞活力至20.09%并诱导了83.82%的亡.
  • 结合疗法导致细胞内GSH和ATP严重耗尽,导致代谢疲劳和细胞毒性增加.
  • 在体内,FCA-PDT-RT在降低RT剂量 (12Gy) 中实现了优异的瘤控制,增加了CD3+/CD8+T细胞透,并抑制了血管新生,并具有良好的安全性.

结论:

  • 通过顺序重塑瘤微环境,放大氧化应激,并诱导代谢疲劳,FCA使PDT-RT协同发挥作用.
  • 这种纳米平台提供了一种剂量节约策略,具有巨大的转化潜力,用于乳腺癌治疗.
  • 以FCA为媒介的组合疗法显示出一种有希望的方法来克服治疗耐药性并改善患者的治疗结果.