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Quantifying Antibody-Dependent Cellular Cytotoxicity in a Tumor Spheroid Model: Application for Drug Discovery
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High-Dose Sunitinib Accelerates Triple-Negative Breast Cancer Metastasis by Modulating an Immunosuppressive

Chen Liu1, Junsheng Xue1, Tianyu Wang1

  • 1Department of Pharmaceutics, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing, 100191, China.

Pharmaceutical Research
|May 27, 2026
PubMed
Summary

High-dose sunitinib (SUN) promotes triple-negative breast cancer (TNBC) metastasis by suppressing the immune microenvironment, not by affecting cancer cell motility. Combining SUN with anti-PD-1 therapy may overcome this resistance.

Keywords:
cancer metastasisdrug resistancesunitinibtriple negative breast cancertumor microenvironment

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Area of Science:

  • Oncology
  • Immunology
  • Pharmacology

Background:

  • Sunitinib (SUN), a tyrosine kinase inhibitor, affects tumor microenvironment (TME) but shows limited benefit in triple-negative breast cancer (TNBC).
  • Drug resistance in TNBC may be linked to SUN's pro-metastatic effects, with unclear dose-dependency and mechanisms.
  • This study investigates the biphasic effect of SUN on metastasis driven by TME alterations at different doses.

Purpose of the Study:

  • To elucidate the dose-dependent effect of sunitinib on triple-negative breast cancer (TNBC) metastasis.
  • To investigate the underlying mechanisms of sunitinib-induced metastasis, focusing on the tumor microenvironment (TME).
  • To explore potential therapeutic strategies to overcome sunitinib resistance in TNBC.

Main Methods:

  • Utilized 4T1 murine TNBC cells and an orthotopic allograft model to assess tumor progression.
  • Examined 4T1 cell motility in vitro using scratch wound and Transwell assays.
  • Analyzed TME changes in vivo via flow cytometry, blood routine analysis, and combined drug evaluations.

Main Results:

  • High-dose sunitinib (SUN) exhibited a pro-metastatic effect in mice without improving survival.
  • High-dose SUN induced an immunosuppressive TME, impairing innate and adaptive immune responses.
  • Co-administration with anti-PD-1 antibody reversed high-dose SUN-induced metastasis, suggesting PD-L1 mediated T-cell inhibition.

Conclusions:

  • Therapeutic dosage of SUN significantly impacts TNBC progression and treatment outcomes.
  • SUN demonstrates a biphasic effect on metastasis, dependent on dosage and TME modulation.
  • Findings suggest optimized therapeutic regimens involving SUN dosage and immunotherapy for TNBC patients.