DEC1 promotes hypoxia-induced epithelial-mesenchymal transition (EMT) in human hepatocellular carcinoma cells

被引:19
|
作者
Murakami, Keishu [1 ]
Wu, Yunyan [1 ]
Imaizumi, Tadaatsu [2 ]
Aoki, Yuka [1 ]
Liu, Qiang [1 ]
Yan, Xu [1 ]
Seino, Hiroko [1 ]
Yoshizawa, Tadashi [1 ]
Morohashi, Satoko [1 ]
Kato, Yukio [3 ]
Kijima, Hiroshi [1 ]
机构
[1] Hirosaki Univ, Grad Sch Med, Dept Pathol & Biosci, 5 Zaifu Cho, Hirosaki, Aomori 0368562, Japan
[2] Hirosaki Univ, Grad Sch Med, Dept Vasc Biol, Hirosaki, Aomori 0368562, Japan
[3] Hiroshima Univ, Inst Biomed & Hlth Sci, Dept Dent & Med Biochem, Hiroshima 7348553, Japan
来源
BIOMEDICAL RESEARCH-TOKYO | 2017年 / 38卷 / 04期
关键词
UP-REGULATION; EXPRESSION; HIF-1-ALPHA;
D O I
10.2220/biomedres.38.221
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Differentiated embryonic chondrocyte (DEC) 1 has been reported to be involved in cell differentiation, hypoxia response, and cancer progression. Recent studies have demonstrated that hypoxia-inducible factor (HIF)-1 alpha induces epithelial-mesenchymal transition (EMT) in carcinoma cells to facilitate cell invasiveness and metastasis. However, it remains unclear whether DEC1 participates in hypoxia-mediated EMT processes. In the present study, we reported that hypoxia induced DEC1 expression in hepatocellular carcinoma (HCC) HepG2 cells, and DEC1 negatively regulated expression of HIF-1 alpha and E-cadherin in transcriptional/translational levels. Cell morphological changes were evaluated with hematoxylin and eosin (H-E) staining. Exposure to hypoxia caused spindle-like shape in some of the HepG2 cells, and DEC1 overexpression furthered these changes. In conclusions, DEC1 is involved in hypoxia-induced EMT processes via negatively regulating E-cadherin expression in HepG2 cells.
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页码:221 / 227
页数:7
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