ArticleAging cell2019
Senescence-associated tissue microenvironment promotes colon cancer formation through the secretory factor GDF15.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02328677 (ColoCare Transdisciplinary Research in Colorectal Cancer Prognosis), which is not on this map. Cited by 88 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
ColoCare Transdisciplinary Research in Colorectal Cancer Prognosis
Who cites it
88 citing papers in PubMed, 126 citations in OpenAlex.
- Effect of menopausal hormone therapy on proteins associated with senescence and inflammation.Physiological reports · 2020Trial
- Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.Biomarker research · 2026Review
- p21-senescent cells drive pancreatic islet dysfunction through targetable paracrine signaling in type 2 diabetes.JCI insight · 2026Article
- Targeting the CAF-GDF15 axis attenuates AKT-mediated mitochondrial rewiring and chemoradiation resistance in esophageal adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Article
- Tumor-derived GDF15 induces CCN3⁺ Schwann cells to promote cancer pain in pancreatic cancer.Nature communications · 2026Article
- GDF15 in aging, metabolic disease and cachexia.The journal of nutrition, health & aging · 2026Article
- Macrophage-Derived PDGF-BB and GDF-15 Promote Drug Resistance in KRAS-Mutant Colorectal Cancer.bioRxiv : the preprint server for biology · 2026Article
- Harnessing Anthocyanins to Mitigate Inflammation, Dysbiosis, and Aging in the Gastrointestinal Tract.ACS pharmacology & translational science · 2026Review
- The Senescence-SASP Landscape in Colon Adenocarcinoma: Prognostic and Therapeutic Implications.Current issues in molecular biology · 2026Article
- Senescent fibroblasts drive CD8Journal of translational medicine · 2026Article
- Of Barriers and Loops-How Evolution Limits Most Cancer Risks to Older Ages.Cancer discovery · 2026Review
- Cellular senescence in precancer lesions and early-stage cancers.Cancer cell · 2026Review
- Decoding the tumor-aging axis: from bench to clinical.Frontiers in immunology · 2026Review
- A Distinct Host-Microbiome Signature Underlies the Accelerated Malignant Potential of Colorectal Laterally Spreading Tumors.Gastro hep advances · 2026Article
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Aging and the extracellular matrix: A tumor-permissive microenvironment driving cancer progression.Current opinion in biomedical engineering · 2025Article
- Peritumoral colonic epithelial cell-derived GDF15 sustains colorectal cancer via regulation of glycolysis and histone lactylation.Nature aging · 2025Article
- Review
- The controversial role of senescence-associated secretory phenotype (SASP) in cancer therapy.Molecular cancer · 2025Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
The risk of colorectal cancer (CRC) varies between people, and the cellular mechanisms mediating the differences in risk are largely unknown. Senescence has been implicated as a causative cellular mechanism for many diseases, including cancer, and may affect the risk for CRC. Senescent fibroblasts that accumulate in tissues secondary to aging and oxidative stress have been shown to promote cancer formation via a senescence-associated secretory phenotype (SASP). In this study, we assessed the role of senescence and the SASP in CRC formation. Using primary human colon tissue, we found an accumulation of senescent fibroblasts in normal tissues from individuals with advanced adenomas or carcinomas in comparison with individuals with no polyps or CRC. In in vitro and ex vivo model systems, we induced senescence using oxidative stress in colon fibroblasts and demonstrated that the senescent fibroblasts secrete GDF15 as an essential SASP factor that promotes cell proliferation, migration, and invasion in colon adenoma and CRC cell lines as well as primary colon organoids via the MAPK and PI3K signaling pathways. In addition, we observed increased mRNA expression of GDF15 in primary normal colon tissue from people at increased risk for CRC in comparison with average risk individuals. These findings implicate the importance of a senescence-associated tissue microenvironment and the secretory factor GDF15 in promoting CRC formation.
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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.