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Peer-reviewedCC BY-NC-NDJournal of translational medicine

Single-cell and spatial transcriptomics reveal that THBS1 induces radiation resistance in TNBC through the interaction between myCAF and TOPBP1⁺ tumor cells.

  1. 1Department of Biochemistry and Molecular Biology, Tianjin Medical University Cancer Hospital, No. 1, Huanhu West Road, Tiyuan North Road, Hexi District, Tianjin, 300060, China.
  2. 2Tianjin Medical University, Tianjin, 300060, China.
  3. 3Department of Biochemistry and Molecular Biology, Tianjin Medical University Cancer Hospital, No. 1, Huanhu West Road, Tiyuan North Road, Hexi District, Tianjin, 300060, China. [email protected].

Abstract

Background

Radiation resistance remains a clinical challenge in the treatment of triple-negative breast cancer (TNBC) and its mechanisms are not yet fully understood.Methods

We integrated single-cell RNA sequencing, spatial transcriptomics, and prognostic data to perform analyses such as intercellular communication, pseudo-temporal trajectories, and GSEA and validated the results using experiments including qPCR, single-cell sequencing and flow cytometry.Results

This study identified a unique subpopulation of epithelial cells, designated TOPBP1⁺ E.T. cells, which retain normal epithelial transcriptional profiles and are associated with poor patient prognosis. myCAF communicates with this cell cluster via the THBS1 signaling pathway, activating the NOTCH signaling pathway to promote resistance to radiotherapy.Conclusions

THBS1 plays a pivotal role in mediating radioresistance in triple-negative breast cancer, positioning it as a promising therapeutic target.

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BibTeX
@article{liu2026singlecell,
  title = {{Single-cell and spatial transcriptomics reveal that THBS1 induces radiation resistance in TNBC through the interaction between myCAF and TOPBP1⁺ tumor cells.}},
  author = {Fuzhong Liu and Xing Xu and Wenhao Tong and Yang Xie and Yecheng Ma and Lingling Yang and Xun Jin},
  journal = {Journal of translational medicine},
  year = {2026},
  month = jul,
  doi = {10.1186/s12967-026-08614-z},
  url = {https://europepmc.org/article/MED/42902364},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Single-cell and spatial transcriptomics reveal that THBS1 induces radiation resistance in TNBC through the interaction between myCAF and TOPBP1⁺ tumor cells.
AU  - Fuzhong Liu
AU  - Xing Xu
AU  - Wenhao Tong
AU  - Yang Xie
AU  - Yecheng Ma
AU  - Lingling Yang
AU  - Xun Jin
PY  - 2026
DA  - 2026/07/01
JO  - Journal of translational medicine
DO  - 10.1186/s12967-026-08614-z
UR  - https://europepmc.org/article/MED/42902364
AB  - Background  Radiation resistance remains a clinical challenge in the treatment of triple-negative breast cancer (TNBC) and its mechanisms are not yet fully understood.Methods  We integrated single-cell RNA sequencing, spatial transcriptomics, and prognostic data to perform analyses such as intercellular communication, pseudo-temporal trajectories, and GSEA and validated the results using experiments including qPCR, single-cell sequencing and flow cytometry.Results  This study identified a unique subpopulation of epithelial cells, designated TOPBP1⁺ E.T. cells, which retain normal epithelial transcriptional profiles and are associated with poor patient prognosis. myCAF communicates with this cell cluster via the THBS1 signaling pathway, activating the NOTCH signaling pathway to promote resistance to radiotherapy.Conclusions  THBS1 plays a pivotal role in mediating radioresistance in triple-negative breast cancer, positioning it as a promising therapeutic target.
SN  - 1479-5876
ER  -