ArticleInternational journal of molecular sciences2024
The Differential Effect of Senolytics on SASP Cytokine Secretion and Regulation of EMT by CAFs.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Role of the stromal and immune microenvironment in intrahepatic cholangiocarcinoma.JHEP reports : innovation in hepatology · 2026Review
- Diosmetin Modulates EMT-Associated Plasticity and Fibroblast-Activation Markers in Parallel Breast Cancer In Vitro Models.Molecules (Basel, Switzerland) · 2026Article
- Single-cell analysis reveals an endothelial TP53-CXCL14 axis in breast cancer progression.Journal of translational medicine · 2026Article
- Thymoquinone and pentoxifylline modulate 5-fluorouracil-induced senescence and apoptosis in colorectal cancer spheroids.Research in pharmaceutical sciences · 2026Article
- The Implications of Radiotherapy-Induced Cellular Senescence for Cancer Treatment and Tumor Microenvironment Modulation.International journal of biological sciences · 2026Review
- Immunosenescence modulates radiation-induced anti-tumor immunity: implications for personalized immuno-oncology.Frontiers in immunology · 2026Review
- Senescence-associated and immune-related 9p21.3 locus genes in colorectal cancer: epigenetic architecture, molecular landscape and therapeutic possibilities.Frontiers in cell and developmental biology · 2026Review
- Apiin Promotes Healthy Aging inInternational journal of molecular sciences · 2025Article
- The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.Molecular cancer · 2025Review
- Accelerated Aging in Cancer and Cancer Treatment: Current Status of Biomarkers.Cancer medicine · 2025Review
- Reciprocal Modulation of Tumour and Immune Cell Motility: Uncovering Dynamic Interplays and Therapeutic Approaches.Cancers · 2025Review
- Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.Molecular cancer · 2025Review
- Harnessing the tumor microenvironment: targeted cancer therapies through modulation of epithelial-mesenchymal transition.Journal of hematology & oncology · 2025Review
- Beyond polarization: macrophage senescence in immunoregulation and cancer therapy.International journal of biological sciences · 2025Review
- Cancer-associated fibroblasts: dual roles from senescence sentinels to death regulators and new dimensions in therapy.Frontiers in immunology · 2025Review
- Metabolic reprogramming and immunosenescence in colorectal cancer: mechanisms and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Targeting Cellular Senescence for Healthy Aging: Advances in Senolytics and Senomorphics.Drug design, development and therapy · 2025Review
- PP2C phosphatases-terminators of suicidal thoughts.Cell death & disease · 2024Review
- Addition of Polyphenols to Drugs: The Potential of Controlling "Inflammaging" and Fibrosis in Human Senescent Lung Fibroblasts In Vitro.International journal of molecular sciences · 2024Article
- Emerging Roles of Vitamin BInternational journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The tumor microenvironment (TME) plays an essential role in tumor progression and in modulating tumor response to anticancer therapy. Cellular senescence leads to a switch in the cell secretome, characterized by the senescence-associated secretory phenotype (SASP), which may regulate tumorigenesis. Senolytic therapy is considered a novel anticancer strategy that eliminates the deleterious effects of senescent cells in the TME. Here, we show that two different types of senolytic drugs, despite efficiently depleting senescent cells, have opposite effects on cancer-associated fibroblasts (CAFs) and their ability to regulate epithelial-mesenchymal transition (EMT). We found that senolytic drugs, navitoclax and the combination of dasatinib/quercetin, reduced the number of spontaneously senescent and TNF-induced senescent CAFs. Despite the depletion of senescent cells, the combination of dasatinib/quercetin versus navitoclax increased the secretion of the SASP pro-inflammatory cytokine IL-6. This differential effect correlated with the promotion of enhanced migration and EMT in MC38 colorectal cancer cells. Our results demonstrate that some senolytics may have side effects unrelated to their senolytic activity and may promote tumorigenesis. We argue for more careful and extensive studies of the effects of senolytics on various aspects of tumor progression and tumor resistance to therapy before the senolytic strategy is implemented in the clinic.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.