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Periostin Mediates the Increased Pro-Angiogenic Activity of Gastric Cancer Cells under Hypoxic Conditions

Authors

  • Feng Qiu,

    1. Department of Oncology, First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People's Republic of China
    2. Affiliated Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China
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  • Chun-hua Shi,

    1. Jiangxi People's Hospital, Nanchang, Jiangxi, People's Republic of China
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  • Jun Zheng,

    1. Department of General Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, People's Republic of China
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  • Yu-bin Liu

    Corresponding author
    1. Department of General Surgery, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, People's Republic of China
    • Jiangxi People's Hospital, Nanchang, Jiangxi, People's Republic of China
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  • Feng Qiu and Chun-hua Shi contributed equally to this work.

Correspondence to: Yu-bin Liu.

ABSTRACT

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

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