ArticleCancer research2016
Cancer-Associated Fibroblasts in Pancreatic Cancer Are Reprogrammed by Tumor-Induced Alterations in Genomic DNA Methylation.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
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Who cites it
84 citing papers in PubMed, 112 citations in OpenAlex.
- Tumor microenvironment evaluation promotes precise checkpoint immunotherapy of advanced gastric cancer.Journal for immunotherapy of cancer · 2021Trial
- Molecular mechanisms and therapeutic strategies: DNA methylation in pancreatic cancer.Cancer biology & therapy · 2026Review
- Review
- The role of epigenetic modifications in cancer-associated fibroblasts.Frontiers in medicine · 2026Review
- The Heterogeneity and Function of Stromal Cells in the Tumor Microenvironment.Research (Washington, D.C.) · 2026Review
- STAT3 signaling in cancer: mechanisms and targeting therapeutic.Frontiers in immunology · 2026Review
- The tumour microenvironment in pancreatic cancer - new clinical challenges, but more opportunities.Nature reviews. Clinical oncology · 2025Review
- Epigenetic reprogramming as the nexus of cancer stemness and therapy resistance: implications for biomarker discovery.Discover oncology · 2025Review
- Significance of Epigenetic Alteration in Cancer-Associated Fibroblasts on the Development of Carcinoma.International journal of molecular sciences · 2025Review
- Stroma and lymphocytes identified by deep learning are independent predictors for survival in pancreatic cancer.Scientific reports · 2025Article
- Tumor suppressor genes in the tumor microenvironment.Disease models & mechanisms · 2025Review
- The multi-faceted roles of cancer-associated fibroblasts in pancreatic cancer.Cellular signalling · 2025Review
- Cancer-associated fibroblasts in carcinogenesis.Journal of translational medicine · 2025Review
- Epigenetic Regulation of Stromal and Immune Cells and Therapeutic Targets in the Tumor Microenvironment.Biomolecules · 2025Review
- Cancer-associated fibroblasts: heterogeneity, tumorigenicity and therapeutic targets.Molecular biomedicine · 2024Review
- Epigenetic regulation of the tumor microenvironment: A leading force driving pancreatic cancer.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024Review
- Glucocorticoids in lung cancer: Navigating the balance between immunosuppression and therapeutic efficacy.Heliyon · 2024Review
- CAFs-Associated Genes (CAFGs) in Pancreatic Ductal Adenocarcinoma (PDAC) and Novel Therapeutic Strategy.International journal of molecular sciences · 2024Review
- Decoding the Tumour Microenvironment: Molecular Players, Pathways, and Therapeutic Targets in Cancer Treatment.Cancers · 2024Review
- Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Stromal fibrosis is a prominent histologic characteristic of pancreatic ductal adenocarcinoma (PDAC), but how stromal fibroblasts are regulated in the tumor microenvironment (TME) to support tumor growth is largely unknown. Here we show that PDAC cells can induce DNA methylation in cancer-associated fibroblasts (CAF). Upon direct contact with PDAC cells, DNA methylation of SOCS1 and other genes is induced in mesenchymal stem cells or in CAF that lack SOCS1 methylation at baseline. Silencing or decitabine treatment to block the DNA methylation enzyme DNMT1 inhibited methylation of SOCS1. In contrast, SOCS1 gene methylation and downregulation in CAF activated STAT3 and induced insulin-like growth factor-1 expression to support PDAC cell growth. Moreover, CAF facilitated methylation-dependent growth of PDAC tumor xenografts in mice. The ability of patient-derived CAF with SOCS1 methylation to promote PDAC growth was more robust than CAF without SOCS1 methylation. Overall, our results reveal how PDAC cells can reprogram CAF to modify tumor-stromal interactions in the TME, which promote malignant growth and progression. Cancer Res; 76(18); 5395-404. ©2016 AACR.
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