Publication: Periostin activates integrin α5β1 through a PI3K/AKT-dependent, pathway in invasion of cholangiocarcinoma
Issued Date
2012-09-01
Resource Type
ISSN
17912423
10196439
10196439
Other identifier(s)
2-s2.0-84864981474
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
International Journal of Oncology. Vol.41, No.3 (2012), 1110-1118
Suggested Citation
Kusumawadee Utispan, Jumaporn Sonongbua, Peti Thuwajit, Siri Chau-In, Chawalit Pairojkul, Sopit Wongkham, Chanitra Thuwajit Periostin activates integrin α5β1 through a PI3K/AKT-dependent, pathway in invasion of cholangiocarcinoma. International Journal of Oncology. Vol.41, No.3 (2012), 1110-1118. doi:10.3892/ijo.2012.1530 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/13624
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Periostin activates integrin α5β1 through a PI3K/AKT-dependent, pathway in invasion of cholangiocarcinoma
Other Contributor(s)
Abstract
Periostin (PN) is mainly produced from stromal fibroblasts in cholangiocarcinoma (CCA) and shows strong impact in cancer promotion. This work aimed to investigate the mechanism that PN uses to drive CCA invasion. It was found that ITGα5β1 and α6β4 showed high expression in non-tumorigenic biliary epithelial cells and in almost all CCA cell lines. PN had preferential binding to CCA cells via ITGα5β1 and blocking this receptor by either neutralizing antibody or siITGα5 could attenuate PN-induced invasion. After PN-ITGα5β1 binding, intracellular pAKT was upregulated whereas there was no change in pERK. Moreover, PN could not activate AKT in condition of treatment with a PI3K inhibitor. These data provide evidence that PN-activated invasion of CCA cells is through the ITGα5β1/PI3K/AKT pathway. Strategies aimed to inhibit this pathway may, thus, provide therapeutic benefits.