Syndecan‐2 is a key regulator of transforming growth factor beta 2/smad2‐mediated adhesion in fibrosarcoma cells

Fibrosarcoma is a rare malignant tumor originating from fibroblasts. Transforming growth factor beta 2 (TGFβ2) has been established to regulate processes correlated to fibrosarcoma tumorigenesis. In this study, we investigated the possible participation of syndecan‐2 (SDC‐2), a cell membrane heparan...

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Published in:IUBMB life 2013-02, Vol.65 (2), p.134-143
Main Authors: Mytilinaiou, Maria, Bano, Artan, Nikitovic, Dragana, Berdiaki, Aikaterini, Voudouri, Kallirroi, Kalogeraki, Alexandra, Karamanos, Nikos K., Tzanakakis, George N.
Format: Article
Language:English
Subjects:
Actins - metabolism
Cell Adhesion
Cell adhesion & migration
Cell Line, Tumor
Fibronectins - metabolism
Fibrosarcoma
Gene Expression
Gene Knockdown Techniques
Humans
Integrin beta1 - genetics
Integrin beta1 - metabolism
Protein Multimerization
Protein Transport
Proteins
Receptors, Transforming Growth Factor beta - genetics
Receptors, Transforming Growth Factor beta - metabolism
RNA, Small Interfering - genetics
Smad2
Smad2 Protein - metabolism
Syndecan-2 - genetics
Syndecan-2 - metabolism
syndecan‐2
Transforming Growth Factor beta2 - physiology
transforming growth factor‐β2 signaling
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Summary:Fibrosarcoma is a rare malignant tumor originating from fibroblasts. Transforming growth factor beta 2 (TGFβ2) has been established to regulate processes correlated to fibrosarcoma tumorigenesis. In this study, we investigated the possible participation of syndecan‐2 (SDC‐2), a cell membrane heparan sulfate (HS) proteoglycan on these TGFβ2 functions. Our results demonstrate that the inhibition of SDC‐2 expression by short interfering RNA (siSDC2) abolished TGFβ2‐dependent HT1080 cell adhesion (P ≤ 0.01). In parallel, the downregulation of SDC‐2 significantly inhibited TGFβ2‐induced Smad2 phosphorylation (P ≤ 0.01). The immunoflourescence signal of TGF receptor III as well as its protein expression was decreased in SDC‐2‐deficient cells. The enhancement of adhesion molecules integrin β1 (P ≤ 0.01) and focal adhesion kinase expression, induced by TGFβ2 treatment (P ≤ 0.001), was markedly inhibited in SDC‐2‐defficient cells (P ≤ 0.01). Conclusively, the obtained data suggest that SDC‐2 modulates TGFβ2 transcriptional regulation via Smad signaling to facilitate fibrosarcoma cell adhesion. © 2013 IUBMB Life, 65(2)134–143, 2013
ISSN:1521-6543
1521-6551
DOI:10.1002/iub.1112