ArticleThe American journal of pathology2006
Platelet-derived growth factor-BB controls epithelial tumor phenotype by differential growth factor regulation in stromal cells.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 62 citations in OpenAlex.
- Combined MEK/PD-L1 Inhibition Alters Peripheral Cytokines and Lymphocyte Populations Correlating with Improved Clinical Outcomes in Advanced Biliary Tract Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Trial
- Role of PDGF-BB in Oral Squamous Cell Carcinoma through PI3/AKT/mTOR Pathway: An Integrated Computational and Real-Time PCR-Based Approach.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Functional and clinical roles of stromal PDGF receptors in tumor biology.Cancer metastasis reviews · 2024Review
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- Cannabidiolic acid in Hemp Seed Oil Table Spoon and Beyond.Molecules (Basel, Switzerland) · 2022Article
- An Interleukin-4 and Interleukin-13 Induced Atopic Dermatitis Human Skin Equivalent Model by a Skin-On-A-Chip.International journal of molecular sciences · 2022Article
- MicroRNA-432-5p regulates sprouting and intussusceptive angiogenesis in osteosarcoma microenvironment by targeting PDGFB.Laboratory investigation; a journal of technical methods and pathology · 2021Article
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- Mechanisms for Reducing Neuropathic Pain.Molecular neurobiology · 2020Review
- Injury-Induced Effectors of Neuropathic Pain.Molecular neurobiology · 2020Review
- Human neonatal stem cell-derived skin substitute improves healing of severe burn wounds in a rat model.Cell biology international · 2019Article
- BMP7 Signaling inMolecular cancer research : MCR · 2018Article
- Immature truncated O-glycophenotype of cancer directly induces oncogenic features.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Differential effects of sorafenib on liver versus tumor fibrosis mediated by stromal-derived factor 1 alpha/C-X-C receptor type 4 axis and myeloid differentiation antigen-positive myeloid cell infiltration in mice.Hepatology (Baltimore, Md.) · 2014Article
- The high angiogenic activity in very early breast cancer enables reliable imaging with VEGFR2-targeted microbubbles (BR55).European radiology · 2013Article
- Shared gene expression alterations in prostate cancer and histologically benign prostate from patients with prostate cancer.The American journal of pathology · 2012Article
- Characterization of the cytokine profile of platelet rich plasma (PRP) and PRP-induced cell proliferation and migration: Upregulation of matrix metalloproteinase-1 and -9 in HaCaT cells.The Korean journal of hematology · 2011Article
- Significantly high expression of platelet-derived growth factor (PDGF) in benign nodules of the thyroid: relevance in the development of goitre recurrence?Langenbeck's archives of surgery · 2011Article
- Platelet-Derived Growth Factor (PDGF)/PDGF Receptors (PDGFR) Axis as Target for Antitumor and Antiangiogenic Therapy.Pharmaceuticals (Basel, Switzerland) · 2010Review
- Platelet-derived growth factor-B normalizes micromorphology and vessel function in vascular endothelial growth factor-A-induced squamous cell carcinomas.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelet-derived growth factor (PDGF) stimulates tumor growth and progression by affecting tumor and stromal cells. In the HaCaT skin carcinogenesis model, transfection of immortal nontumorigenic and PDGF-receptor-negative HaCaT keratinocytes with PDGF-B induced formation of benign tumors. Here, we present potential mechanisms underlying this tumorigenic conversion. In vivo, persistent PDGF-B expression induced enhanced tumor cell proliferation but only transiently stimulated stromal cell proliferation and angiogenesis. In vitro and in vivo studies identified fibroblasts as PDGF target cells essential for mediating transient angiogenesis and persistent epithelial hyperproliferation. In fibroblast cultures, long-term PDGF-BB treatment caused an initial up-regulation of vascular endothelial growth factor (VEGF)-A, followed by a drastic VEGF down-regulation and myofibroblast differentiation. Accordingly, in HaCaT/PDGF-B transplants, initially enhanced VEGF expression by stromal fibroblasts was subsequently reduced, followed by down-regulation of angiogenesis, myofibroblast accumulation, and vessel maturation. The PDGF-induced, persistently increased expression of the hepatocyte growth factor by fibroblasts in vitro and in vivo was most probably responsible for enhanced epithelial cell proliferation and benign tumor formation. Thus, by paracrine stimulation of the stroma, PDGF-BB induced epithelial hyperproliferation, thereby promoting tumorigenicity, whereas the time-limited activation of the stroma followed by stromal maturation provides a possible explanation for the benign tumor phenotype.
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