Document Detail


Transforming growth factor beta1 produced in autocrine/paracrine manner affects the morphology and function of mesothelial cells and promotes peritoneal carcinomatosis.
MedLine Citation:
PMID:  20664947     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Human peritoneal mesothelial cells (HPMCs) in intact mesothelium have been demonstrated to protect against tumor peritoneal metastasis. We have previously reported that gastric cancer cells can induce peritoneal apoptosis, lead to damage of peritoneum integrity, and therefore promote peritoneal metastasis. In this study, we investigated the effects of TGF-beta1 on tumor-mesothelial interaction. Briefly, the levels of various soluble factors, in particular TGF-beta1, were measured. HMrSV5 cells, a human peritoneal mesothelial cell line, were co-incubated with TGF-beta1, gastric cancer cells, or gastric cancer cells and TGF-beta1 receptor inhibitor SB431542. The expressions of smad 2/3 and phosphorylated smad 2/3, indicator of TGF-beta/Smads pathway activation, were evaluated. Then the morphological changes of HPMCs were observed. The cell damage was quantitatively determined by fluorescent microscopy and flow cytometry. Tumor-mesothelial cell adhesion was also examined. Results showed a significant elevation of TGF-beta1 expression, which is companied by dramatically increased phosphorylated-smad 2/3 levels, after mesothelial cell co-culture with the gastric cancer cell line. In addition, mesothelial cells exposed to gastric cancer cells or TGF-beta1 became exfoliated and exhibited signs of injury, while blocking TGF-beta1 can partially inhibit these effects. These results indicate that soluble factors, such as TGF-beta1, produced in autocrine/paracrine manner in the peritoneal cavity, affect the morphology and function of mesothelial cells so that the resulting environment becomes favorable for peritoneal metastases.
Authors:
Di Na; Zhi-Dong Lv; Fu-Nan Liu; Yan Xu; Cheng-Gang Jiang; Zhe Sun; Zhi-Feng Miao; Feng Li; Hui-Mian Xu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  International journal of molecular medicine     Volume:  26     ISSN:  1791-244X     ISO Abbreviation:  Int. J. Mol. Med.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-07-28     Completed Date:  2010-11-04     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9810955     Medline TA:  Int J Mol Med     Country:  Greece    
Other Details:
Languages:  eng     Pagination:  325-32     Citation Subset:  IM    
Affiliation:
Department of Surgical Oncology, The First Affiliated Hospital, China Medical University, Shenyang, Liaoning Province, PR China.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / physiology
Autocrine Communication / physiology*
Benzamides / metabolism
Carcinoma* / pathology,  physiopathology
Cell Adhesion / physiology
Cell Shape
Cells, Cultured
Coculture Techniques
Culture Media, Conditioned
Culture Media, Serum-Free
Dioxoles / metabolism
Epithelial Cells* / cytology,  metabolism
Epithelium / metabolism*
Humans
Neoplasm Metastasis
Paracrine Communication / physiology*
Peritoneal Neoplasms* / pathology,  physiopathology,  secondary
Receptors, Transforming Growth Factor beta / antagonists & inhibitors
Stomach Neoplasms* / metabolism,  pathology
Transforming Growth Factor beta1 / genetics,  metabolism*
Chemical
Reg. No./Substance:
0/4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide; 0/Benzamides; 0/Culture Media, Conditioned; 0/Culture Media, Serum-Free; 0/Dioxoles; 0/Receptors, Transforming Growth Factor beta; 0/Transforming Growth Factor beta1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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