miR-210，一种卵巢癌细胞中缺氧诱导上皮-间质转化的调节因子。
miR-210, a modulator of hypoxia-induced epithelial-mesenchymal transition in ovarian cancer cell.
作者信息
Ding Lu, Zhao Le, Chen Wei, Liu Ting, Li Zhen, Li Xu
机构信息
Center for Translational Medicine, First Affiliated Hospital, Xi'an Jiaotong University College of Medicine Xi'an, P.R. China.
Center for Laboratory Medicine, First Affiliated Hospital, Xi'an Jiaotong University College of Medicine Xi'an, P.R. China.
出版信息
Int J Clin Exp Med. 2015 Feb 15;8(2):2299-307. eCollection 2015.
Abstract
miR-210 has been found consistently induced by hypoxia and implicated in cancer progression. Despite widespread exploration on miR-210 function, little is known about its action on invasion and metastasis of ovarian cancer. In this study, miR-210 was induced by hypoxia in SKOV3 ovarian cancer cells and then suppressed with its specific inhibitor. Repression of miR-210 in hypoxic cells led to upregulation of E-cadherin, downregulation of vimentin and Snail, and attenuation of wound healing capability. On the other hand, miR-210 was overexpressed in normoxic SKOV3 cells, which resulted in decrease of E-cadherin, increase of vimentin and Snail, and facilitation of wound healing capability. These results revealed that miR-210 promoted ovarian cancer cell mobility by acting as a modulator of epithelial-mesenchymal transition (EMT), highlighting the importance of miR-210 in ovarian cancer progression.
摘要
已发现miR-210在缺氧状态下持续被诱导，并与癌症进展有关。尽管对miR-210的功能进行了广泛研究，但对其在卵巢癌侵袭和转移方面的作用却知之甚少。在本研究中，miR-210在SKOV3卵巢癌细胞中由缺氧诱导产生，然后用其特异性抑制剂进行抑制。在缺氧细胞中抑制miR-210导致E-钙黏蛋白上调、波形蛋白和Snail下调，以及伤口愈合能力减弱。另一方面，miR-210在常氧SKOV3细胞中过表达，导致E-钙黏蛋白减少、波形蛋白和Snail增加，以及伤口愈合能力增强。这些结果表明，miR-210通过作为上皮-间质转化（EMT）的调节因子促进卵巢癌细胞的迁移，突出了miR-210在卵巢癌进展中的重要性。
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