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Prolyl hydroxylase 3 inhibited the tumorigenecity of gastric cancer cells
Author(s) -
Cui Lei,
Qu Jianguo,
Dang Shengchun,
Mao Zhengfa,
Wang Xuqing,
Fan Xin,
Sun Kang,
Zhang Jianxin
Publication year - 2014
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.22025
Subject(s) - biology , cancer , cancer research , cancer cell , biochemistry , medicine , genetics
Gastric cancer is one of the most common malignancies and the second leading cause of cancer‐related death in the world, and it is very urgent to develop novel therapeutic strategies. Although HIF‐1α is the most highly characterized target of prolyl hydroxylase 3 (PHD3), PHD3 has been shown to regulate several signal pathways independent of HIF‐1α. Here, we found that the expression of PHD3 was decreased in the clinical gastric cancer samples and reversely correlated with tumor size and tumor stage. Over‐expression of PHD3 in the gastric cancer cells significantly inhibited cell growth in vitro and in vivo, while knockdown the expression of PHD3 promoted the tumorigenecity of gastric cancer cells. Mechanistically, it showed that PHD3 downregulated the expression of beta‐catenin and inhibited beta‐catenin/T‐cell factor (TCF) signaling. Taken together, our findings demonstrate that PHD3 inhibits gastric cancer by suppressing the beta‐catenin/TCF signaling and PHD3 might be an important therapeutic target in gastric cancer. Copyright © 2013 Wiley Periodicals, Inc.