ArticleOncology reports2023
The impact of cellular senescence and senescence‑associated secretory phenotype in cancer‑associated fibroblasts on the malignancy of pancreatic cancer.
Article in Oncology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Ketogenic Diet as an Adjuvant in Epithelial Cancers: Mechanisms, Model Systems, and Translational Opportunities.Cancers · 2026Review
- Brain metastasis-associated fibroblasts shape the tumour microenvironment to enhance cancer cell invasion.Brain pathology (Zurich, Switzerland) · 2026Article
- Cellular senescence in cancer: Unveiling dual roles, tumor microenvironment dynamics and therapeutic innovations (Review).Oncology letters · 2025Review
- The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.Molecular cancer · 2025Review
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Immunosenescence and cancer: molecular hallmarks, tumor microenvironment remodeling, and age-specific immunotherapy challenges.Journal of hematology & oncology · 2025Review
- Crosstalk between cancer‑associated fibroblasts and inflammation in tumor microenvironment: A novel perspective in cancer therapy (Review).Oncology reports · 2025Review
- Fibroblast atlas: Shared and specific cell types across tissues.Science advances · 2025Article
- Patient-Derived Cancer-Associated Fibroblasts Support the Colonization of Tumor Cells in Head and Neck Squamous Cell Carcinoma.Biomedicines · 2025Article
- Cancer-associated fibroblasts: dual roles from senescence sentinels to death regulators and new dimensions in therapy.Frontiers in immunology · 2025Review
- p53: A player in the tumor microenvironment.Oncology research · 2025Review
- Extracellular Vesicles in Ovarian Cancer: From Chemoresistance Mediators to Therapeutic Vectors.Biomedicines · 2024Review
- Regulation of ENPP5, a senescence-associated secretory phenotype factor, prevents skin aging.Biogerontology · 2024Article
- Integrative Analysis and Validation of a Cancer-associated Fibroblasts Senescence-related Signature for Risk Stratification and Therapeutic Prediction in Esophageal Squamous Cell Carcinoma.Journal of Cancer · 2024Article
- Modulation of tumor plasticity by senescent cells: Deciphering basic mechanisms and survival pathways to unravel therapeutic options.Genetics and molecular biology · 2024Article
- The hidden messengers: cancer associated fibroblasts-derived exosomal miRNAs as key regulators of cancer malignancy.Frontiers in cell and developmental biology · 2024Review
- Characterization of cancer-associated fibroblasts (CAFs) and development of a CAF-based risk model for triple-negative breast cancer.Cancer cell international · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer‑associated fibroblasts (CAFs) are implicated in the strong malignancy of pancreatic cancer (PC). Various CAF subtypes have different functions, and their heterogeneity likely influence the malignancy of PC. Meanwhile, it is known that senescent cells can create a tumor‑promoting microenvironment by inducing a senescence‑associated secretory phenotype (SASP). In the present study, the effects of individual differences in CAFs on PC malignancy were investigated with a focus on cellular senescence. First, primary cultures of CAFs from 8 PC patients were generated and co‑cultured with PC cell lines. This co‑culture assay showed that differences in CAFs induce differences in PC cell proliferation. It was further investigated which clinical factors affected the malignant potential of CAF and it was found that the difference of malignant potential of each CAF was marginally related to the age of original patients. Next, to verify the senescence of CAFs really affected the malignant potential of CAF, PCR array analysis of each CAF sample was performed and it was revealed that expression of genes about cellular senescence and SASP such as tumor protein p53, nuclear factor kappa B subunit 1, and IL6, are related to the malignant potential of CAFs impacting on PC proliferation. Finally, to elucidate the effect of p53‑mediated cellular senescence of CAFs on malignant potential of PC, it was examined whether CAFs with the treatment of p53 inhibitor affected PC cell proliferation in co‑culture assays. The treatment of CAFs with p53 inhibitor significantly suppressed PC cell proliferation. In addition, a comparison of the concentration of IL‑6, a SASP cytokine, in the co‑culture supernatant showed a significant decrease in the sample after p53 inhibitor treatment. In conclusion, the present results suggested that proliferation potential of PC may be related to p53‑mediated cellular senescence and SASP of CAFs.
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