ArticleThe Biochemical journal2002
The role of syndecan-2 in regulation of actin-cytoskeletal organization of Lewis lung carcinoma-derived metastatic clones.
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- SDC2 and FN as cargo proteins in circulating extracellular vesicles in obese breast cancer patients with lymph node metastasis.Scientific reports · 2025Article
- Heparan sulfate proteoglycans in cancer: Pathogenesis and therapeutic potential.Advances in cancer research · 2023Article
- Matrix proteoglycans in tumor inflammation and immunity.American journal of physiology. Cell physiology · 2022Review
- miR-218 affects the ECM composition and cell biomechanical properties of glioblastoma cells.Journal of cellular and molecular medicine · 2022Article
- Joint Secondary Transcriptomic Analysis of Non-Hodgkin's B-Cell Lymphomas Predicts Reliance on Pathways Associated with the Extracellular Matrix and Robust Diagnostic Biomarkers.Journal of bioinformatics and systems biology : Open access · 2022Article
- Identification of an immune-related signature indicating the dedifferentiation of thyroid cells.Cancer cell international · 2021Article
- Syndecans and Pancreatic Ductal Adenocarcinoma.Biomolecules · 2021Review
- Heparan Sulfate Proteoglycan Signaling in Tumor Microenvironment.International journal of molecular sciences · 2020Review
- Syndecan-2: Old Player in a New Field.American journal of respiratory cell and molecular biology · 2019Article
- Lung Adenocarcinoma Syndecan-2 Potentiates Cell Invasiveness.American journal of respiratory cell and molecular biology · 2019Article
- Article
- Fell-Muir Lecture: Syndecans: from peripheral coreceptors to mainstream regulators of cell behaviour.International journal of experimental pathology · 2015Review
- Heparan Sulfate Proteoglycans May Promote or Inhibit Cancer Progression by Interacting with Integrins and Affecting Cell Migration.BioMed research international · 2015Review
- Syndecans as modulators and potential pharmacological targets in cancer progression.Frontiers in oncology · 2014Review
- Neuroendocrine tumors show altered expression of chondroitin sulfate, glypican 1, glypican 5, and syndecan 2 depending on their differentiation grade.Frontiers in oncology · 2014Article
- Syndecan-2 is upregulated in colorectal cancer cells through interactions with extracellular matrix produced by stromal fibroblasts.BMC cell biology · 2013Article
- Syndecan-2 promotes perineural invasion and cooperates with K-ras to induce an invasive pancreatic cancer cell phenotype.Molecular cancer · 2012Article
- Antithetic roles of proteoglycans in cancer.Cellular and molecular life sciences : CMLS · 2012Review
- Proteoglycans in cancer biology, tumour microenvironment and angiogenesis.Journal of cellular and molecular medicine · 2011Review
- Syndecan-2 functions as a docking receptor for pro-matrix metalloproteinase-7 in human colon cancer cells.The Journal of biological chemistry · 2009Article
Corrections and comments
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8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Syndecans, a family of transmembrane heparan sulphate proteoglycans, contribute to various biological processes, including adhesion, motility, proliferation, differentiation and morphogenesis. We document here the involvement of syndecan-2 acting alone or co-operatively with integrin alpha5beta1, for regulation of actin-cytoskeletal organization on cell adhesion to fibronectin, using fibronectin-recombinant polypeptides containing the ligands for either or both of these receptors as substrata. Lewis lung carcinoma-derived low-metastatic P29 cells binding to the substrata by both receptors formed actin stress fibres, whereas those binding by syndecan-2 or integrin alpha5beta1 alone formed filopodia or cortex actin. In contrast, higher metastatic LM66-H11 cells formed cortex actin even on substrata containing both ligands. Northern-blot and flow-cytometric analyses revealed that syndecan-2 expression in LM66-H11 cells was significantly lower (1/4.5 in mRNA and 1/8 in cell-surface expression) than in P29 cells, whereas expression levels of integrin alpha5beta1 and other syndecans were similar in both cell types. These results suggest that the failure of LM66-H11 to form stress fibres is due to a lower expression of syndecan-2 than that due to a threshold for its function. This was confirmed by the finding that overexpression of syndecan-2 by transfection of its cDNA into LM66-H11 cells caused the formation of stress fibres on the fibronectin substratum. These in vitro cellular responses of the two clones might reflect their in vivo situation in primary tumours in which P29 cells with a stroma-inducing capacity were immediately surrounded by fibronectin-rich matrix formed by the induced stromal cells, whereas LM66-H11 cells without such capacity were not surrounded by a similar matrix.
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