期刊
CELLULAR SIGNALLING
卷 26, 期 5, 页码 1011-1020出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2014.01.025
关键词
Focal adhesion kinase; Migration; Tumorigenicity; Transcription
类别
资金
- National Natural Science Foundation of China [81172350, 81272693]
- Program for New Century Talent of the National Ministry of Education, China
- Fundamental Research Funds for the Chinese Central University [201130202020016]
The tumor suppressor gene phosphatase and tensin homolog (PTEN) is essential in inhibiting tumor growth and metastasis. However, the mechanism by which PTEN restricts gastric cancer progression and metastasis remains largely elusive. Here we demonstrated that PTEN overexpression or knockdown in gastric cancer cells led to the downregulation or upregulation of focal adhesion kinase (FAK), and decreased or increased cell invasion, respectively. Moreover, FAK overexpression could rescue the inhibition of cell invasion by PTEN. These results were further confirmed in orthotropic gastric cancer nude mice model. In addition, in human gastric cancer tissues, PTEN protein level was conversely correlated with FAK protein level. Mechanistically, we found that PTEN inhibited PI3K/NF-kappa B pathway and inhibited the DNA binding of NF-kappa B on FAK promoter. Taken together, our data reveal a novel mechanism that PTEN inhibits the growth and invasion of gastric cancer via the downregulation of FAK expression and suggest that exploiting PTEN/PI3K/NF-kappa B/FAK axis is a promising approach to treat gastric cancer metastasis. Crown Copyright (c) 2014 Published by Elsevier Inc. All rights reserved.
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