ArticleMolecular oncology2016
Biglycan stimulates VEGF expression in endothelial cells by activating the TLR signaling pathway.
Article in Molecular oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.
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Who cites it
70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.
- Chromosome X-wide association study in case control studies of pathologically confirmed Alzheimer's disease in a European population.Translational psychiatry · 2024Pooled it
- Gene expression in stress urinary incontinence: a systematic review.International urogynecology journal · 2020Pooled it
- Spermidine suppresses liver fibrosis by remodeling the communication signal between liver sinusoidal endothelial cells and hepatic stellate cells.Cell death discovery · 2026Article
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- BGN Secreted by Cancer-Associated Fibroblasts Promotes Esophageal Squamous Cell Carcinoma Progression via Activation of TLR4-Mediated Erk and NF-κB Signaling Pathways.International journal of molecular sciences · 2025Article
- Proteoglycans in Breast Cancer: Friends and Foes.Biomolecules · 2025Review
- Proteoglycans and glycosaminoglycans: critical regulators in angiogenesis, vasculogenesis, and vascularized tissue engineering.Angiogenesis · 2025Review
- Biglycan stimulates retinal pathological angiogenesis via up-regulation of CXCL12 expression in pericytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Comprehensive Analysis of Potential Common Pathogenic Mechanisms for COVID-19 Infection and Gastric Cancer.Analytical cellular pathology (Amsterdam) · 2025Article
- Benign non-immune cells in tumor microenvironment.Frontiers in immunology · 2025Review
- The Role of the Pancreatic Extracellular Matrix as a Tissue Engineering Support for the Bioartificial Pancreas.Biomimetics (Basel, Switzerland) · 2024Review
- Toll-like receptors in health and disease.MedComm · 2024Review
- SESN1 functions as a new tumor suppressor gene via Toll-like receptor signaling pathway in neuroblastoma.CNS neuroscience & therapeutics · 2024Article
- Identification of differentially expressed genes associated with the pathogenesis of gastric cancer by bioinformatics analysis.BMC medical genomics · 2023Article
- GRg1 inhibits the TLR4/NF-kB signaling pathway by upregulating miR-216a-5p to reduce growth factors and inflammatory cytokines in DR.Molecular biology reports · 2023Article
- The Landscape of Small Leucine-Rich Proteoglycan Impact on Cancer Pathogenesis with a Focus on Biglycan and Lumican.Cancers · 2023Review
- Pathophysiological mechanism of acute bone loss after fracture.Journal of advanced research · 2023Review
- Developmental diversity and unique sensitivity to injury of lung endothelial subtypes during postnatal growth.iScience · 2023Article
- BGN/FAP/STAT3 positive feedback loop mediated mutual interaction between tumor cells and mesothelial cells contributes to peritoneal metastasis of gastric cancer.International journal of biological sciences · 2023Article
- Doxorubicin-sensitive and -resistant colorectal cancer spheroid models: assessing tumor microenvironment features for therapeutic modulation.Frontiers in cell and developmental biology · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Biglycan (BGN) is an important component of the extracellular matrix (ECM) that is implicated in a variety of human cancers. In our previous study, we reported that BGN was overexpressed in gastric cancer (GC) tissues and promoted cancer metastasis. Moreover, the tubular formation capacity in HUVECs was promoted by stimulation with culture media from BGN-overexpressing GC cells, but the exact underlying mechanism is still unknown. The purpose of this study was to determine the role and molecular mechanism of BGN in VEGF expression in endothelial cells. We found that BGN stimulation of endothelial cells increased the interaction between NF-kB and the HIF-1α promoter, leading to enhanced promoter activity and increased HIF-1α mRNA levels, as well as augmented HIF-1 activity that resulted in VEGF expression. All of this was dependent on the interaction of BGN with its receptors, TLR2 and TLR4. Moreover, we found that BGN enhanced endothelial cell migration and proliferation, as well as tube formation, in a TLR signaling pathway-dependent manner. In addition, endothelial cell-derived VEGF in turn was found to act on GC cells and promotes their migration. The combined findings of our current and previous studies suggest that BGN secreted from GC cells into the tumor stroma promotes GC development, as well as its progression, potentially through the chronic activation of tumor angiogenesis.
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