Murakami Keishu, Wu Yunyan, Imaizumi Tadaatsu, Aoki Yuka, Liu Qiang, Yan Xu, Seino Hiroko, Yoshizawa Tadashi, Morohashi Satoko, Kato Yukio, Kijima Hiroshi
Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine.
Department of Vascular Biology, Hirosaki University Graduate School of Medicine.
Biomed Res. 2017;38(4):221-227. doi: 10.2220/biomedres.38.221.
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.
据报道，分化型胚胎软骨细胞（DEC）1参与细胞分化、缺氧反应和癌症进展。最近的研究表明，缺氧诱导因子（HIF）-1α诱导癌细胞发生上皮-间质转化（EMT），以促进细胞侵袭和转移。然而，DEC1是否参与缺氧介导的EMT过程仍不清楚。在本研究中，我们报道缺氧诱导肝癌（HCC）HepG2细胞中DEC1表达，并且DEC1在转录/翻译水平上负向调节HIF-1α和E-钙黏蛋白的表达。用苏木精和伊红（H-E）染色评估细胞形态变化。暴露于缺氧环境会使一些HepG2细胞呈纺锤状，DEC1过表达会加剧这些变化。总之，DEC1通过负向调节HepG2细胞中E-钙黏蛋白的表达参与缺氧诱导的EMT过程。
