Literature DB >> 28794399

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

Keishu Murakami1, Yunyan Wu1, Tadaatsu Imaizumi2, Yuka Aoki1, Qiang Liu1, Xu Yan1, Hiroko Seino1, Tadashi Yoshizawa1, Satoko Morohashi1, Yukio Kato3, Hiroshi Kijima1.   

Abstract

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)-1α 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-1α 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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Year:  2017        PMID: 28794399     DOI: 10.2220/biomedres.38.221

Source DB:  PubMed          Journal:  Biomed Res        ISSN: 0388-6107            Impact factor:   1.203


  8 in total

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8.  The Mechanisms Underlying the Cytotoxic Effects of Copper Via Differentiated Embryonic Chondrocyte Gene 1.

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  8 in total

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