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Peer-reviewedCC BY 4.0Frontiers in Immunology

Cellular senescence in ovarian cancer: context-dependent effects on tumor immunity and therapy response

  • Yubo Zhang1
  • Mengqi Deng2,3
  • Junyi Jiang4
4 affiliations
  1. 1Qingdao Hospital, University of Health and Rehabilitation Sciences (Qingdao Municipal Hospital)
  2. 2Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing Maternal and Child Health Care Hospital
  3. 3Laboratory for Clinical Medicine, Capital Medical University
  4. 4State Key Laboratory of Medical Proteomics, National Center for Protein Sciences (Beijing)
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Abstract

Cellular senescence is a stress-responsive state marked by sustained proliferative arrest and changes in metabolism, chromatin organization, secretion, and immune signaling. In ovarian cancer (OC), platinum therapy and PARP inhibition can generate senescence-associated states with distinct consequences. Their effects depend on treatment context, cellular compartment, stability of arrest, and the surrounding immune state. Therapy-induced senescent tumor cells may increase antigen presentation and inflammatory signaling and, in immune-competent settings, facilitate dendritic-cell and CD8+ T-cell responses. Persistent senescence can instead maintain a SASP that remodels stromal and immune compartments and may support residual disease, dissemination, or relapse. OC studies have linked altered senescence responses to cisplatin resistance, while senescence-associated states have also been reported after PARP inhibition and taxane treatment. Senescence in CAFs, mesothelial cells, adipose-associated stroma, and immune cells can further alter tumor-cell survival, invasion, immune surveillance, and treatment response. We therefore distinguish stable TIS from reversible senescence-like or dormant states and separate tumor-cell effects from stromal and immune effects. Senolysis, SASP modulation, ferroptosis, and immune-mediated clearance represent potential strategies, but most evidence remains preclinical. Overall, senescence in OC is best viewed as a context-dependent state that can either support antitumor immunity or facilitate immune escape and treatment persistence.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026cellular,
  title = {{Cellular senescence in ovarian cancer: context-dependent effects on tumor immunity and therapy response}},
  author = {Yubo Zhang and Mengqi Deng and Junyi Jiang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1965539},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1965539/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Cellular senescence in ovarian cancer: context-dependent effects on tumor immunity and therapy response
AU  - Yubo Zhang
AU  - Mengqi Deng
AU  - Junyi Jiang
PY  - 2026
DA  - 2026/10/26
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1965539
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1965539/full
AB  - Cellular senescence is a stress-responsive state marked by sustained proliferative arrest and changes in metabolism, chromatin organization, secretion, and immune signaling. In ovarian cancer (OC), platinum therapy and PARP inhibition can generate senescence-associated states with distinct consequences. Their effects depend on treatment context, cellular compartment, stability of arrest, and the surrounding immune state. Therapy-induced senescent tumor cells may increase antigen presentation and inflammatory signaling and, in immune-competent settings, facilitate dendritic-cell and CD8+ T-cell responses. Persistent senescence can instead maintain a SASP that remodels stromal and immune compartments and may support residual disease, dissemination, or relapse. OC studies have linked altered senescence responses to cisplatin resistance, while senescence-associated states have also been reported after PARP inhibition and taxane treatment. Senescence in CAFs, mesothelial cells, adipose-associated stroma, and immune cells can further alter tumor-cell survival, invasion, immune surveillance, and treatment response. We therefore distinguish stable TIS from reversible senescence-like or dormant states and separate tumor-cell effects from stromal and immune effects. Senolysis, SASP modulation, ferroptosis, and immune-mediated clearance represent potential strategies, but most evidence remains preclinical. Overall, senescence in OC is best viewed as a context-dependent state that can either support antitumor immunity or facilitate immune escape and treatment persistence.
SN  - 1664-3224
ER  -