ArticleNature communications2025
Therapy-induced senescent cancer cells contribute to cancer progression by promoting ribophorin 1-dependent PD-L1 upregulation.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Topological Quantum Biomaterials Enable Pyroptosis-Senescence Coupling for Enhanced Colorectal Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Metabolic licensing of quiescent glioblastoma activation and immune evasion via astrocyte-mitochondria shuttle.Nature communications · 2026Article
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- Fate Bifurcation of Cellular Senescence: Dynamic Regulation from Tumor Suppression to Recurrence Risk.Cells · 2026Review
- Radionuclide-labeled oxygen-self-supplying calcium reservoir for high-efficiency radioimmunotherapy via synergistic pyroptosis activation and PD-L1 downregulation.Journal of nanobiotechnology · 2026Article
- Fatty acid synthesis therapy-induced senescence (FASTIS) in cancer cells.Cell death & disease · 2026Article
- Ultrasound-responsive biomimetic nanocarrier triggers spatiotemporal PROTAC release and ROS storm to disrupt TNBC immunosuppression via coordinated apoptosis/ferroptosis/senescence activation.Journal of nanobiotechnology · 2026Article
- Functional and Transcriptional Senescence Profiles of CD8+ T Cells Associate With the Presence of Carotid Plaques in People Living With HIV.The Journal of infectious diseases · 2026Article
- Stress-responsive membrane proteins as execution nodes of tumor cell adaptation to microenvironmental stress.Oncogene · 2026Review
- Therapy-induced senescent cancer cells as bidirectional regulators of antitumor immunity and resistance in the tumor microenvironment.Cell death & disease · 2026Review
- Cellular senescence in lung cancer immune microenvironment and senotherapeutic opportunities.iScience · 2026Review
- Biomimetic Nanomedicine for Senescence-Modulated Immune Activation Enhances Immunotherapy Efficacy in Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Research progress on the spatiotemporal dynamics of therapy-induced senescence in remodeling the tumor microenvironment.Frontiers in immunology · 2026Review
- RPN1 at the crossroads of glycosylation, tumor immunity, and disulfidptosis.Frontiers in pharmacology · 2026Review
- Immunosenescence in prostate cancer: from aging-related immune dysfunction to therapeutic opportunities.Frontiers in immunology · 2026Review
- Breast cancer pathogenesis, diagnosis and treatment: a comprehensive review.Frontiers in oncology · 2026Review
- CDKN1A/p21 Influences the Survival and Expansion of Breast Cancer Stem Cells after Oxidative Damage.Oncology research · 2026Article
- Regulation of glycosylation in radiotherapy: exploring the multiple effects of DNA damage, immune response, stromal microenvironment and metabolism.Frontiers in oncology · 2026Review
- Glycosylated IgG antibodies contribute to the recovery of haemorrhagic fever with renal syndrome patients.eLife · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Conventional chemotherapy- and radiotherapy-induced cancer senescence, which is characterized by poor proliferation, drug resistance, and senescence-associated secretory phenotype, has gained attention as contributing to cancer relapse and the development of an immunosuppressive tumor microenvironment. However, the association between cancer senescence and anti-tumor immunity is not fully understood. Here, we demonstrate that senescent cancer cells increase the level of PD-L1 by promoting its transcription and glycosylation. We identify ribophorin 1 as a key regulator of PD-L1 glycosylation during cancer senescence. Ribophorin 1 depletion reduces this elevated level of PD-L1 through the ER-lysosome-associated degradation pathway, thereby increasing the susceptibility of senescent cancer cells to T-cell-mediated killing. Consistently, ribophorin 1 depletion suppresses tumor growth by decreasing PD-L1 levels and boosting cytotoxic T lymphocyte activity in male mice. Moreover, ribophorin 1-targeted or anti-PD-1 therapy reduces the number of senescent cancer cells in irradiated tumors and suppresses cancer recurrence through the activation of cytotoxic T lymphocytes. These results provide crucial insights into how senescent cancer cells can escape T-cell immunity following cancer treatment and thereby contribute to cancer recurrence. Our findings also highlight the therapeutic promise of targeting senescent cancer cells for cancer treatment.
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