MiR-210 Links Hypoxia With Cell Proliferation Regulation in Human Laryngocarcinoma Cancer
MiR-210 Links Hypoxia With Cell Proliferation Regulation in Human Laryngocarcinoma Cancer
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MiR-210 将缺氧与人喉癌细胞增殖调节联系起来
DOI：
10.1002/jcb.25059
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发表时间：
2015-06-01
影响因子：
4
通讯作者：
Liu, Zhigang
中科院分区：
文献类型：
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作者：
Zuo, Jianhong;Wen, Meiling;Liu, Zhigang
microRNA hsa-miR-210（miR-210）与缺氧相关;然而其功能尚未完全确定。在本研究中，我们的目的是检测其在喉癌增殖中的作用。我们发现miR-210在缺氧条件下高表达，通过诱导细胞周期停滞在G1/G 0期以及凋亡来抑制增殖。我们进一步鉴定了miR-210靶向成纤维细胞生长因子受体样1（FGFRL 1）。下调FGFRL 1表达可使G1/G 0期细胞比例增加，S期和G2/M期细胞比例减少，从而抑制细胞增殖。此外，FGFRL 1的过表达有效地解除了miR-210诱导的SCC 10A细胞增殖抑制。miR-210的表达也抑制了体内肿瘤异种移植物的生长。总之，我们的研究结果揭示了一种新的适应缺氧的机制，即miR-210通过靶向FGFRL 1诱导细胞周期阻滞和凋亡来抑制增殖。(C)2015年威利期刊公司
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.