4.6 Article

19-peptide, a fragment of tumstatin, inhibits the growth of poorly differentiated gastric carcinoma cells in vitro and in vivo

Journal

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY
Volume 25, Issue 5, Pages 935-941

Publisher

WILEY
DOI: 10.1111/j.1440-1746.2009.06209.x

Keywords

cell and molecular biology; gastric cancer: basic experimental study; animal models

Funding

  1. National Natural Science Foundation of China [30472035]
  2. Special Funded Project for Youth [QC05C38]
  3. Key Technology Project [ZJY04-0102]
  4. China Postdoctoral Science Foundation

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Background and Aim: This study investigated whether 19-peptide, a fragment of tumstatin, inhibited the growth of gastric tumor cells in vitro and in vivo. Methods: 19-peptide was expressed in bacteria and purified with Sephadex G-15. SGC7901 gastric carcinoma cells and human umbilical-vein endothelial cells (HUVECs) were exposed to 19-peptide in vitro, and their viability was evaluated by biochemical and histopathological analysis. In vivo, pieces of solid tumor derived from SGC7901 cells were inoculated into the gastric serosa of 36 nude mice, with a biological glue to hold them in place. Twenty-eight days after injection of 19-peptide, the mice were killed. The tumors were measured and examined by western blotting, histopathology, and terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling assay. Results: 19-peptide induced apoptosis of many SGC7901 cells but few HUVECs in vitro. In vivo, after the application of 19-peptide, significant tumor cell apoptosis was observed in the center of the tumors, tumor volume was reduced significantly (P < 0.001), and the invasion and migration of cancer cells was reduced. PTEN was increased in the treatment group and phospho-Akt (pAkt) was decreased in the control group. Conclusions: These results suggest that 19-peptide inhibits the growth and metastases of poorly differentiated gastric carcinoma cells, primarily by inducing apoptosis. The apoptotic mechanism could be related to anoikis and the PTEN/Akt pathway.

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