ArticleThe Journal of biological chemistry2017
Syndecan-2 cytoplasmic domain up-regulates matrix metalloproteinase-7 expression via the protein kinase Cγ-mediated FAK/ERK signaling pathway in colon cancer.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- A study on the correlation between DNA methylation and protein expression levels ofThe Journal of international medical research · 2026Article
- Fibulin-4 and latent-transforming growth factor beta-binding protein-4 interactions with syndecan-2 and syndecan-3 are required for elastogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Redefining metalloproteases specificity through network proteolysis.Trends in molecular medicine · 2024Review
- TCN1 Deficiency Inhibits the Malignancy of Colorectal Cancer Cells by Regulating the ITGB4 Pathway.Gut and liver · 2023Article
- Review
- Substituted Syndecan-2-Derived Mimetic Peptides Show Improved Antitumor Activity over the Parent Syndecan-2-Derived Peptide.International journal of molecular sciences · 2022Article
- Article
- Effects of fluid shear stress on expression of focal adhesion kinase in MG-63 human osteoblast-like cells on different surface modification of titanium.Bioengineered · 2021Article
- Syndecan receptors: pericellular regulators in development and inflammatory disease.Open biology · 2021Review
- Emerging Role of Syndecans in Extracellular Matrix Remodeling in Cancer.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Heparan Sulfate Proteoglycan Signaling in Tumor Microenvironment.International journal of molecular sciences · 2020Review
- Metalloproteinases and Their Inhibitors: Potential for the Development of New Therapeutics.Cells · 2020Review
- microRNA-9 Inhibits Vulnerable Plaque Formation and Vascular RemodelingFrontiers in physiology · 2020Article
- Stromal vascular fraction promotes migration of fibroblasts and angiogenesis through regulation of extracellular matrix in the skin wound healing process.Stem cell research & therapy · 2019Article
- Tyrosine 51 residue of the syndecan-2 extracellular domain is involved in the interaction with and activation of pro-matrix metalloproteinase-7.Scientific reports · 2019Article
- Soluble syndecans: biomarkers for diseases and therapeutic options.British journal of pharmacology · 2019Review
- DKK1 inhibits breast cancer cell migration and invasion through suppression of β-catenin/MMP7 signaling pathway.Cancer cell international · 2019Article
- Analysis of Genes Involved in Ulcerative Colitis Activity and Tumorigenesis Through Systematic Mining of Gene Co-expression Networks.Frontiers in physiology · 2019Article
- Identification of hub genes with diagnostic values in pancreatic cancer by bioinformatics analyses and supervised learning methods.World journal of surgical oncology · 2018Article
- Heparan Sulfate Proteoglycans in Human Colorectal Cancer.Analytical cellular pathology (Amsterdam) · 2018Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The syndecan family of heparan sulfate proteoglycans contributes to cell adhesion and communication by serving as co-receptors for cell signaling and extracellular matrix molecules. Syndecan-2 is located at the cell surface, and we previously reported that it induces matrix metalloproteinase-7 (MMP-7) expression in colon cancer cells. However, the underlying regulatory mechanisms are unknown. Here, we report that overexpression of syndecan-2 in HT-29 colon cancer cells increases the phosphorylation of focal adhesion kinase (FAK) and ERK in parallel with up-regulated MMP-7 expression, but a syndecan-2 mutant lacking the cytoplasmic domain showed significant reductions in these effects. Consistent with this observation, FAK inhibition via FAK-related non-kinase expression or inhibition of ERK with the ERK1/2 inhibitor SCH772984 diminished the syndecan-2-mediated up-regulation of MMP-7. Activation of PKC enhanced syndecan-2-mediated MMP-7 expression, whereas inhibition of PKC had the opposite effect. Of note, the exogenous expression of syndecan-2 triggered localization of PKCγ to the membrane. Expression of syndecan-2 harboring a phosphomimetic (S198E) mutation of the variable region of the cytoplasmic domain enhanced MMP-7 expression and FAK phosphorylation. Finally, experimental suppression of shedding of the syndecan-2 extracellular domain did not significantly affect the syndecan-2-mediated up-regulation of MMP-7 in the early period after syndecan-2 overexpression. Taken together, these findings suggest that syndecan-2's cytoplasmic domain up-regulates MMP-7 expression in colon cancer cells via PKCγ-mediated activation of FAK/ERK signaling.
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