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Dual Sensitization Enables Synergistic Photodynamic Therapy and Radiotherapy for Breast Cancer.

Yingying Zhang1, Shaoqing Chen1, Chun Liu1

  • 1The Second People's Hospital of Changzhou, the Third Affiliated Hospital of Nanjing Medical University; Jiangsu Province Engineering Research Center of Medical Physics; Medical Physics Research Center, Nanjing Medical University; Key Laboratory of Medical Physics in Changzhou, Jiangsu, Changzhou 213003, China.

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Summary
This summary is machine-generated.

This study introduces FCA, a novel nanoplatform that enhances breast cancer treatment by remodeling the tumor microenvironment and amplifying oxidative stress. FCA-photodynamic therapy-radiotherapy (PDT-RT) synergistically combats tumors, offering a promising dose-sparing strategy.

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Area of Science:

  • Biomedical Engineering
  • Nanotechnology
  • Cancer Therapy

Background:

  • Breast cancer treatment using radiotherapy (RT) and photodynamic therapy (PDT) faces limitations due to tumor hypoxia and poor photosensitizer efficacy.
  • Developing advanced nanoplatforms is crucial for overcoming these challenges and improving therapeutic outcomes.

Purpose of the Study:

  • To develop and evaluate a novel folate-modified copper-doped carbon dot nanoplatform (FCA) loaded with 5-aminolevulinic acid (ALA) for synergistic breast cancer treatment.
  • To investigate FCA's ability to remodel the tumor microenvironment, enhance reactive oxygen species (ROS) generation, and sensitize cancer cells to RT and PDT.

Main Methods:

  • Fabrication of FCA nanoplatforms with cascade nanozyme activities for H2O2 decomposition, ROS generation, and glutathione (GSH) depletion.
  • Assessment of FCA's impact on ALA-to-protoporphyrin IX conversion and subsequent ROS amplification.
  • Evaluation of FCA-PDT-RT synergy in reducing 4T1 breast cancer cell viability, inducing apoptosis, and triggering cell cycle arrest.
  • Analysis of the NRF2-KEAP1-HMOX1 pathway activation and metabolic crisis induction.
  • In vivo studies using an orthotopic 4T1 breast cancer model to assess tumor control, immune cell infiltration, angiogenesis, and safety.

Main Results:

  • FCA effectively decomposed H2O2, depleted GSH, and amplified ROS generation, priming the tumor microenvironment.
  • FCA-PDT-RT significantly reduced 4T1 cell viability to 20.09% and induced 83.82% apoptosis, linked to NRF2-KEAP1-HMOX1 pathway activation.
  • The combined therapy caused severe depletion of intracellular GSH and ATP, leading to metabolic exhaustion and enhanced cytotoxicity.
  • In vivo, FCA-PDT-RT achieved superior tumor control at a reduced RT dose (12 Gy), increased CD3+/CD8+ T cell infiltration, and suppressed angiogenesis with favorable safety.

Conclusions:

  • FCA enables synergistic PDT-RT by sequentially remodeling the tumor microenvironment, amplifying oxidative stress, and inducing metabolic exhaustion.
  • This nanoplatform offers a dose-sparing strategy with significant translational potential for breast cancer therapy.
  • FCA-mediated combination therapy demonstrates a promising approach to overcome treatment resistance and improve patient outcomes.