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 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