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首页> 外文期刊>Journal of cellular biochemistry. >MiR-210 Links Hypoxia With Cell Proliferation Regulation in Human Laryngocarcinoma Cancer
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MiR-210 Links Hypoxia With Cell Proliferation Regulation in Human Laryngocarcinoma Cancer

机译:MiR-210将缺氧与人类喉癌的细胞增殖调控联系起来

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摘要

The microRNA hsa-miR-210 (miR-210) is associated with hypoxia; however its function has not fully identified. In the present study, we aim to detect its role concerning proliferation in Laryngocarcinoma. We found that miR-210 was highly expressed in hypoxia, which inhibited proliferation by inducing cell cycle arrest in G1/G0 as well as apoptosis. We further identified that miR-210 targeted fibroblast growth factor receptor-like 1 (FGFRL1). Down regulation of FGFRL1 decreased cell proliferation by promoting proportion of cells in G1/G0 phase and decreasing in S and G2/M phases. Moreover, overexpression of FGFRL1 effectively released the miR-210-induced suppression of SCC10A cell proliferation. Expression of miR-210 repressed tumor xenograft growth in vivo as well. Together, our findings reveal a new mechanism of adaptation to hypoxia that miR-210 inhibits the proliferation via inducing cell cycle arrest and apoptosis by the targeting of FGFRL1. (C) 2015 Wiley Periodicals, Inc.
机译:microRNA hsa-miR-210(miR-210)与缺氧有关;但是,其功能尚未完全确定。在本研究中,我们旨在检测其在喉癌中的增殖作用。我们发现miR-210在缺氧状态下高度表达,通过诱导G1 / G0的细胞周期停滞以及凋亡来抑制增殖。我们进一步确定了miR-210靶向成纤维细胞生长因子受体样1(FGFRL1)。 FGFRL1的下调通过促进G1 / G0期的细胞比例并降低S和G2 / M期的细胞比例来降低细胞增殖。此外,FGFRL1的过表达有效释放了miR-210诱导的SCC10A细胞增殖抑制。 miR-210的表达也抑制体内肿瘤异种移植物的生长。在一起,我们的发现揭示了一种适应缺氧的新机制,即miR-210通过靶向FGFRL1诱导细胞周期停滞和凋亡来抑制增殖。 (C)2015威利期刊公司

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