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Peer-reviewedCC BY 4.0Frontiers in Oncology

JAK-STAT signaling: a key mechanism of immune microenvironment remodeling in breast cancer and novel strategies for targeted therapy

  • Junfang Qiao1,2
  • Tingting Sun1,2
  • Guoqiang Wang1,2
  • Ying Yan2,3
  • Weibing Tong2
  1. 1Graduate School of Inner Mongolia Medical University
  2. 2Breast Tumor Center, Beijing University Cancer Hospital Inner Mongolia Hospital
  3. 3Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Breast Oncology, Peking University Cancer Hospital and Institute
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Abstract

The JAK-STAT signaling pathway serves as a critical hub for cytokine signal transduction, and its aberrant activation plays a decisive role in shaping the immune microenvironment of breast cancer. This review systematically elucidates how this pathway contributes to the construction of an immunosuppressive microenvironment through upregulating PD-L1 expression, recruiting and activating myeloid-derived suppressor cells (MDSCs), promoting regulatory T cell (Treg) generation, while concomitantly suppressing the functions of CD8+ T cells and natural killer (NK) cells. Although targeted therapy against this pathway, particularly in combination with immune checkpoint inhibitors, has demonstrated promising potential, several challenges remain, including pathway compensation, low inhibitor selectivity, associated toxicities, and the lack of predictive biomarkers. Future directions should focus on the development of highly selective STAT inhibitors, exploration of immunophenotype-guided combination strategies, establishment of robust biomarker systems, and in-depth investigation of the dynamic interplay between this pathway and the immune microenvironment, thereby providing a theoretical foundation for combined immunotherapy in breast cancer.

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Cite

BibTeXRIS
BibTeX
@article{qiao2026jakstat,
  title = {{JAK-STAT signaling: a key mechanism of immune microenvironment remodeling in breast cancer and novel strategies for targeted therapy}},
  author = {Junfang Qiao and Tingting Sun and Guoqiang Wang and Ying Yan and Weibing Tong},
  journal = {Frontiers in Oncology},
  year = {2026},
  month = oct,
  doi = {10.3389/fonc.2026.1947188},
  url = {https://www.frontiersin.org/articles/10.3389/fonc.2026.1947188/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - JAK-STAT signaling: a key mechanism of immune microenvironment remodeling in breast cancer and novel strategies for targeted therapy
AU  - Junfang Qiao
AU  - Tingting Sun
AU  - Guoqiang Wang
AU  - Ying Yan
AU  - Weibing Tong
PY  - 2026
DA  - 2026/10/20
JO  - Frontiers in Oncology
DO  - 10.3389/fonc.2026.1947188
UR  - https://www.frontiersin.org/articles/10.3389/fonc.2026.1947188/full
AB  - The JAK-STAT signaling pathway serves as a critical hub for cytokine signal transduction, and its aberrant activation plays a decisive role in shaping the immune microenvironment of breast cancer. This review systematically elucidates how this pathway contributes to the construction of an immunosuppressive microenvironment through upregulating PD-L1 expression, recruiting and activating myeloid-derived suppressor cells (MDSCs), promoting regulatory T cell (Treg) generation, while concomitantly suppressing the functions of CD8+ T cells and natural killer (NK) cells. Although targeted therapy against this pathway, particularly in combination with immune checkpoint inhibitors, has demonstrated promising potential, several challenges remain, including pathway compensation, low inhibitor selectivity, associated toxicities, and the lack of predictive biomarkers. Future directions should focus on the development of highly selective STAT inhibitors, exploration of immunophenotype-guided combination strategies, establishment of robust biomarker systems, and in-depth investigation of the dynamic interplay between this pathway and the immune microenvironment, thereby providing a theoretical foundation for combined immunotherapy in breast cancer.
SN  - 2234-943X
ER  -