Volume 13 Issue 5, October 2003: 343-350
ORIGINAL ARTICLES
TGF-β1-promoted epithelial-to-mesenchymal transformation and cell adhesion contribute to TGF-β1-enhanced cell migration in SMMC-7721 cells
ZHEN XU1, MIN XIONG SHEN2, DONG ZHU MA1, LI YING WANG1, XI LIANG ZHA1*
1Key Laboratory of Glycoconjugate Research, Ministry of Public Health, Department of Biochemistry and Molecular Biology, Shanghai Medical College, Fudan University, Shanghai 200032, China. Email: xlzha@shmu.edu.cn
2Medical School, Huzhou Teacher's College, Huzhou Zhejiang 313000, China
Correspondence: Xi Liang ZHA
Transforming growth factor-β (TGF-β), a multi-function polypeptide, is a double-edged
sword in cancer. For some tumor cells, TGF-β is a potent growth inhibitor and
apoptosis inducer. More commonly, TGF-β loses its growth-inhibitory and apoptosis-inducing
effects, but stimulates the metastatic capacity of tumor cells. It is currently
little known about TGF-β-promoted cell migration in hepatocellular carcinoma
(HCC) cells, let alone its mechanism. In this study, we found that TGF-β lost
its tumor-suppressive effects, but significantly stimulated cell migration in
SMMC-7721 human HCC cells. By FACS and Western blot analysis, we observed that
TGF-β enhanced the expression of
a5β
integrin obviously, and subsequently stimulated cell adhesion onto fibronectin
(Fn). Furthermore, we observed that TGF-β could also promote SMMC-7721 cells
adhesion onto laminin (Ln). Our data also provided evidences that TGF-β induced
epithelial-to-mesenchymal transformation (EMT) in SMMC-7721 cells. First, SMMC-7721
cells clearly switched to the spindle shape morphology after TGF-β treatment.
Furthermore, TGF-β induced the down-regulation of E-cadherin and the nuclear
translocation of βcatenin. These results indicated that TGF-β-promoted cell
adhesion and TGF-β-induced epithelial-to-mesenchymal transformation might be
both responsible for TGF-β-enhanced cell migration.
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