Feng Qiu and Chun-hua Shi contributed equally to this work.
Periostin Mediates the Increased Pro-Angiogenic Activity of Gastric Cancer Cells under Hypoxic Conditions
Article first published online: 31 MAY 2013
© 2013 Wiley Periodicals, Inc.
Journal of Biochemical and Molecular Toxicology
Volume 27, Issue 7, pages 364–369, July 2013
How to Cite
Qiu, F., Shi, C.-h., Zheng, J. and Liu, Y.-b. (2013), Periostin Mediates the Increased Pro-Angiogenic Activity of Gastric Cancer Cells under Hypoxic Conditions. J. Biochem. Mol. Toxicol., 27: 364–369. doi: 10.1002/jbt.21498
- Issue published online: 2 JUL 2013
- Article first published online: 31 MAY 2013
- Manuscript Accepted: 3 MAY 2013
- Manuscript Received: 17 MAR 2013
- Gastric Cancer;
- Vascular Endothelial Growth Factor;
This study was conducted to investigate the biological role of periostin in gastric cancer (GC) under hypoxia. Western blot analysis revealed that along with an upregulation of hypoxia-inducible factor-1alpha, there was a time-dependent induction of periostin in MKN-45 cells under hypoxia (2% O2), increasing by eightfold as compared to normoxic cells. Pretreatment with 30 µM PD98059, an inhibitor of ERK1/2, significantly reduced hypoxia-stimulated periostin expression (P < 0.01). Periostin knockdown in MKN-45 cells was achieved by specific small interfering RNA (siRNA). The conditioned medium from periostin siRNA-transfected MKN-45 cells induced significantly less (P < 0.01) endothelial tube formation than control siRNA-transfected cells. Additionally, periostin silencing markedly decreased the mRNA expression and secretion of vascular endothelial growth factor (VEGF) in hypoxic MKN-45 cells. Thus, our data suggest that periostin is a hypoxia-response gene and mediates a cross talk between GC and endothelial cells under hypoxia, partially through regulation of the VEGF expression. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:364-369, 2013; View this article online at wileyonlinelibrary.com. DOI 10.1002/jbt.21498