ArticleMolecular cancer2025
Therapy-induced senescence is a transient drug resistance mechanism in breast cancer.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.GeroScience · 2026Article
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Lactylation-Driven PROS1-TYRO3-CARF Signaling Promotes Therapy-Induced Senescence Escape and Radioresistance in Meningioma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Fate Bifurcation of Cellular Senescence: Dynamic Regulation from Tumor Suppression to Recurrence Risk.Cells · 2026Review
- Tilting the balance of life and death: navigating DNA replication stress in cancer therapy.Experimental & molecular medicine · 2026Review
- Reframing cancer drug resistance: transporters, persister cells, senescence, and emerging therapeutic strategies.Magyar onkologia · 2026Review
- Postbiotics as Emerging Strategy Targeting Obesity- and Aging-Related Breast Cancer-Prospects in Prophylaxis and Therapy.Life (Basel, Switzerland) · 2026Review
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
- Molecular profiling of glioblastoma-derived extracellular vesicles identifies small nucleolar RNAs as candidate liquid biomarkers for radiation- induced senescence.bioRxiv : the preprint server for biology · 2026Article
- Fluorescent properties of FDA-approved anti-leukemia drugs.Biomedical optics express · 2026Article
- Precision targeting of the SASP in cancer therapy.Nature aging · 2026Article
- Algorithm-assisted individualized therapy design improves survival in a mouse model of triple-negative breast cancer.NPJ precision oncology · 2026Article
- CircRNA14781 promotes olaparib resistance of ovarian cancer cells by regulating miR-330-5p/NGFR pathway.Journal of ovarian research · 2026Article
- Cancer cells surviving cisplatin chemotherapy increase stress-induced OMA1 activity and mitochondrial fragmentation.Scientific reports · 2026Article
- ALYREF-mediated mInternational journal of biological sciences · 2026Article
- Differential responses to the combination of navitoclax and venetoclax with doxorubicin in murine models of triple negative breast cancer.Frontiers in cell and developmental biology · 2026Article
- Dendritic Cell Therapy in Immuno-Oncology: A Potentially Key Component of Anti-Cancer Immunotherapies.Cancers · 2025Review
- Optimization of Methods for the Quantitative Analysis of Global Cell Surface Proteome and Cell Surface Polarization.International journal of molecular sciences · 2025Article
- Unleashing endogenous regeneration by senolytics.Journal of translational medicine · 2025Review
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16 authors.
Funding
Abstract
backgroundTherapy-induced senescence (TIS) is considered a permanent cell cycle arrest following DNA-damaging treatments; however, its irreversibility has recently been challenged. Here, we demonstrate that escape from TIS is universal across breast cancer cells. Moreover, TIS provides a reversible drug resistance mechanism that ensures the survival of the population, and could contribute to relapse.
methodsTIS was induced in four different breast cancer cell line with high-dose chemotherapy and cultured until cells escaped TIS. Parental, TIS and repopulating cells were analyzed by bulk and single-cell RNA sequencing and surface proteomics. A genetically engineered mouse model of triple-negative breast cancer was used to prove why current senolytics cannot overcome TIS in tumors.
resultsScreening the toxicity of a diverse panel of FDA-approved anticancer drugs revealed that TIS meditates resistance to half of these compounds, despite their distinct mechanism of action. Bulk and single-cell RNA sequencing, along with surface proteome analysis, showed that while parental and repopulating cells are almost identical, TIS cells are significantly different from both, highlighting their transient nature. Furthermore, investigating dozens of known drug resistance mechanisms offered no explanation for this unique drug resistance pattern. Additionally, TIS cells expressed a gene set associated with immune evasion and a potential KRAS-driven escape mechanism from TIS.
conclusionOur results reveal that TIS, as a transient drug resistance mechanism, could contribute to overcome the immune response and to relapse by reverting to a proliferative stage.
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