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Peer-reviewedCC BY 4.0Frontiers in Molecular Biosciences

Macrophage reprogramming by the ultraviolet filter benzophenone-1 promotes malignant phenotypes in breast cancer cells: integrated computational and experimental evidence

  • Binglu He1,2
  • Longying Ding3
  • Xiaolu Yang1,2
  • Tianqi Zhang1,2
  • Li Ma1
  1. 1Department of Breast Disease Center, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, China
  2. 2Hebei Medical University, Shijiazhuang, China
  3. 3College of Veterinary Medicine, Shandong Agricultural University, Tai’an, China
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Abstract

Background: Benzophenone-1 (BP-1) is a benzophenone ultraviolet absorber used in cosmetic and personal care products. Although BP-1 exhibits estrogenic activity, its broader effects in breast cancer remain unclear. This study investigated the molecular and cellular responses associated with BP-1 exposure.

Methods: Integrated computational analyses were used to identify core targets and determine their cellular distribution. Molecular modeling evaluated BP-1–target binding. Macrophage polarization and secretion were assessed by immunofluorescence, RT-qPCR, enzyme-linked immunosorbent assay, and western blotting. The effects of macrophage-conditioned medium on breast cancer cells were examined using proliferation, migration, invasion, and epithelial-mesenchymal transition assays.

Results: PLAUR was identified as the core BP-1-related candidate and was prominently expressed in macrophages. BP-1 increased expression of uPAR, the protein encoded by PLAUR, and shifted macrophages toward an M2-like phenotype. Conditioned medium from these macrophages enhanced malignant phenotypes in breast cancer cells.

Conclusion: This study identifies a macrophage-associated response to BP-1 exposure that may contribute to malignant phenotypes in estrogen receptor-positive breast cancer, with PLAUR/uPAR as a candidate mediator. These findings provide a basis for further mechanistic and in vivo studies.

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Cite

BibTeXRIS
BibTeX
@article{he2026macrophage,
  title = {{Macrophage reprogramming by the ultraviolet filter benzophenone-1 promotes malignant phenotypes in breast cancer cells: integrated computational and experimental evidence}},
  author = {Binglu He and Longying Ding and Xiaolu Yang and Tianqi Zhang and Li Ma},
  journal = {Frontiers in Molecular Biosciences},
  year = {2026},
  month = oct,
  doi = {10.3389/fmolb.2026.1946836},
  url = {https://doi.org/10.3389/fmolb.2026.1946836},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Macrophage reprogramming by the ultraviolet filter benzophenone-1 promotes malignant phenotypes in breast cancer cells: integrated computational and experimental evidence
AU  - Binglu He
AU  - Longying Ding
AU  - Xiaolu Yang
AU  - Tianqi Zhang
AU  - Li Ma
PY  - 2026
DA  - 2026/10/13
JO  - Frontiers in Molecular Biosciences
DO  - 10.3389/fmolb.2026.1946836
UR  - https://doi.org/10.3389/fmolb.2026.1946836
AB  - Background: Benzophenone-1 (BP-1) is a benzophenone ultraviolet absorber used in cosmetic and personal care products. Although BP-1 exhibits estrogenic activity, its broader effects in breast cancer remain unclear. This study investigated the molecular and cellular responses associated with BP-1 exposure.  Methods: Integrated computational analyses were used to identify core targets and determine their cellular distribution. Molecular modeling evaluated BP-1–target binding. Macrophage polarization and secretion were assessed by immunofluorescence, RT-qPCR, enzyme-linked immunosorbent assay, and western blotting. The effects of macrophage-conditioned medium on breast cancer cells were examined using proliferation, migration, invasion, and epithelial-mesenchymal transition assays.  Results: PLAUR was identified as the core BP-1-related candidate and was prominently expressed in macrophages. BP-1 increased expression of uPAR, the protein encoded by PLAUR, and shifted macrophages toward an M2-like phenotype. Conditioned medium from these macrophages enhanced malignant phenotypes in breast cancer cells.  Conclusion: This study identifies a macrophage-associated response to BP-1 exposure that may contribute to malignant phenotypes in estrogen receptor-positive breast cancer, with PLAUR/uPAR as a candidate mediator. These findings provide a basis for further mechanistic and in vivo studies.
SN  - 2296-889X
ER  -