Relieving immunosuppression during long-term anti-angiogenesis therapy using photodynamic therapy and oxygen delivery

Qianyuan He1, Zhanjie Zhang1, Haojie Liu2

  • 1Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. jin@hust.edu.cn yangkunyu@medmail.com.cn.

Nanoscale
|July 7, 2020
PubMed

Insights

This study introduces SCM@BSA, a novel nanocarrier for cancer therapy. It improves anti-angiogenesis drugs, enhances solubility, and combats the immunosuppressive tumor microenvironment (TME).

Area of Science:

  • Biomedical Engineering
  • Nanotechnology
  • Cancer Therapeutics

Background:

  • Anti-angiogenesis therapy is crucial for cancer treatment but faces limitations like poor drug solubility and efficacy.
  • Long-term anti-angiogenesis can worsen tumor hypoxia and immune suppression within the tumor microenvironment (TME).

Purpose of the Study:

  • To develop a single nanocarrier agent that overcomes the limitations of traditional anti-angiogenesis monotherapy.
  • To co-deliver an anti-angiogenic drug, a photosensitizer, and an oxygen supply to the tumor site.
  • To reshape the immunosuppressive TME during anti-angiogenic therapy.

Main Methods:

  • Formulation of a bovine serum albumin nanocarrier (SCM@BSA) co-delivering Sorafenib (S), Ce6 (C), and MnO2 (M).
  • Evaluation of SCM@BSA's solubility, therapeutic effects, and impact on the TME compared to monotherapy.

Main Results:

  • SCM@BSA demonstrated improved solubility and therapeutic outcomes compared to anti-angiogenesis monotherapy.
  • The nanocarrier effectively reshaped the immunosuppressive TME.
  • A simple synthesis method yielded a potent nanoscale therapeutic agent.

Conclusions:

  • SCM@BSA offers a promising solution to the shortcomings of long-term anti-angiogenic therapy.
  • This nanocarrier system enhances drug delivery and modulates the tumor microenvironment for improved cancer treatment.
  • The developed agent addresses hydrophobicity and low therapeutic effects of anti-angiogenesis drugs.

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