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Syndecan‐2 is a key regulator of transforming growth factor beta 2/smad2‐mediated adhesion in fibrosarcoma cells
Author(s) -
Mytilinaiou Maria,
Bano Artan,
Nikitovic Dragana,
Berdiaki Aikaterini,
Voudouri Kallirroi,
Kalogeraki Alexandra,
Karamanos Nikos K.,
Tzanakakis George N.
Publication year - 2013
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.1112
Subject(s) - ht1080 , syndecan 1 , fibrosarcoma , smad , transforming growth factor , cell adhesion , microbiology and biotechnology , chemistry , integrin , signal transduction , growth factor , cell growth , cell adhesion molecule , focal adhesion , downregulation and upregulation , small interfering rna , cancer research , cell , biology , transfection , receptor , biochemistry , genetics , gene
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