ArticlePharmaceutical research2026
High-Dose Sunitinib Accelerates Triple-Negative Breast Cancer Metastasis by Modulating an Immunosuppressive Microenvironment: A Preclinical 4T1 Model Study.
Article in Pharmaceutical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Therapeutic potential and mechanisms of rehabilitation interventions in preventing cancer metastasis.Frontiers in oncology · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSunitinib (SUN), a multi-targeted anti-angiogenic tyrosine kinase inhibitor, could inhibit tumor growth and affect tumor microenvironment (TME). However, survival benefit for triple-negative breast cancer (TNBC) patients was limited and the drug resistance probably related to its pro-metastatic effect. The association between metastasis progression and SUN dosage, also the underlying mechanism still remains unclear. Herein, we illustrated the biphasic effect of SUN on metastasis attributed to divergent TME conditions modulated by different therapeutic SUN doses.
methods4T1 murine TNBC cells and orthotopic allograft model were used. The effect of different doses of SUN on tumor progression was assessed on tumor-bearing mice. Mechanistically, scratch wound assay and Transwell were used to examine the motility of 4T1 cells in vitro. Flow cytometry, blood routine and combined drug evaluation were conducted to explore the TME-related pro-metastatic mechanism in vivo.
resultsWithin therapeutic range, only high-dose SUN demonstrated pro-metastatic effect and have no benefit on prolonging the mice survival. Notably, it induced an immunosuppressive TME in multi-sites attenuating both innate and adaptive immune response rather than altering 4T1 cells motility. Consistent with the PD-L1 mediated T-cell inhibition in primary TME, co-administration of an anti-programmed death-1 (PD-1) monoclonal antibody reversed the high-dose SUN-induced increase in metastasis.
conclusionsOur data critically elaborated the impact of therapeutic dosage of SUN on tumor progression and treatment outcome. Our finding emphasized the biphasic effect under diverse SUN dosages and potentially informed optimized therapeutic regimens for TNBC patients.
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