title: [Role of transforming growth factor-β1 in epithelial-mesenchymal transition of mesothelial cells and its effect on peritoneal metastasis of gastric cancer].
abstract: OBJECTIVE
  To elucidate the role of transforming growth factor-beta1(TGF-β1) in epithelial-mesenchymal transition of mesothelial cells and peritoneal metastasis of gastric cancer.
  
  
  METHODS
  HMrSV5 cells, a human peritoneal mesothelial cell line, were incubated with TGF-β1, and their morphological changes were observed by phase contrast microscopy. Expressions of α-smooth muscle actin (α-SMA), vimentin, cytokeratin, E-cadherin, phosphorylated-Smad2 and Smad2 were examined by Western blotting. After fibroblastic-like mesothelial cells were co-incubate with HSC-39 cells(gastric cancer cell line), the adhesion and invasion potential of HSC-39 were evaluated by adhesion and invasion assay in vitro.
  
  
  RESULTS
  Few mesothelial cells converted to spindle fibroblast-like morphology for 24 h, and remarkable phenotypic changes were observed at 72 h of TGF-β1 activation. TGF-β1 could induce α-SMA and vimentin expression, and down-regulate cytokeratin and E-cadherin expression in mesothelial cells (P<0.05). TGF-β1 induced phosphorylation of Smad2 within 15 min of stimulation, reached a maximum at 30 min after treatment and remained high level during the experiment without affecting total Smad2 expression(P>0.05). The percentage of HSC-39 gastric cancer cells adhered were significantly increased as compared to the control. When the mesothelial cells were treated by TGF-β1 for 72 h, the increased adhesion percentage was(146±17)%(P<0.05). After fibroblastic-like mesothelial cells co-incubated with HSC-39 cells for 48 h, more cancer cells [(61.1±11.4) cells/view field] invaded the coated membrane as compared to the control group [(31.9±8.1) cells/view field] (P<0.05).
  
  
  CONCLUSIONS
  TGF-β1 can induce the transition of mesothelial cells into myofibroblasts and Smad2 signal pathway may play a role in this transition, which is associated with increased adhesion and invasiveness of gastric cancer cells, and provides favorable environment for the dissemination of gastric cancer.
authors: Department of Breast Surgery, The Affiliated Hospital, Qingdao University, Qingdao 266003, China. qingyiwhb@126.com.
authors: Zhidong
authors: Z
authors: Lyu
authors: Bin
authors: B
authors: Kong
authors: Xiangping
authors: X
authors: Liu
authors: Funian
authors: F
authors: Li
authors: Haibo
authors: H
authors: Wang
authors: Huimian
authors: H
authors: Xu
mesh_terms: D015820:Cadherins; D045744:Cell Line, Tumor; D004847:Epithelial Cells; D058750:Epithelial-Mesenchymal Transition; D004848:Epithelium; D005347:Fibroblasts; D006801:Humans; D010534:Peritoneal Neoplasms; D015398:Signal Transduction; D051899:Smad2 Protein; D013274:Stomach Neoplasms; D053773:Transforming Growth Factor beta1; D014746:Vimentin
chemical_list: D015820:Cadherins; C497782:SMAD2 protein, human; D051899:Smad2 Protein; D053773:Transforming Growth Factor beta1; D014746:Vimentin