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长链非编码RNA HOTAIR通过靶向miR-193a调控急性髓系白血病中c-KIT的表达。

Long non-coding RNA HOTAIR modulates c-KIT expression through sponging miR-193a in acute myeloid leukemia.

作者信息

Xing Chong-yun, Hu Xiao-qu, Xie Fei-yan, Yu Zhi-jie, Li Hai-ying, Wu Jian-bo, Tang Li-yuan, Gao Shen-meng

机构信息

Department of Hematology, The First Affiliated Hospital of Wenzhou Medical University, Shangcai Village, Nanbaixiang, Ouhai District, Wenzhou, China.

Surgical Oncology, The First Affiliated Hospital of Wenzhou Medical University, Shangcai Village, Nanbaixiang, Ouhai District, Wenzhou, China.

出版信息

FEBS Lett. 2015 Jul 8;589(15):1981-7. doi: 10.1016/j.febslet.2015.04.061. Epub 2015 May 12.

DOI:10.1016/j.febslet.2015.04.061
PMID:25979172
Abstract

HOTAIR is significantly overexpressed in various cancers and facilitates tumor invasion and metastasis. However, whether HOTAIR plays oncogenic roles in acute myeloid leukemia (AML) is still unknown. Here, we report that HOTAIR expression was obviously increased in leukemic cell lines and primary AML blasts. Clinically, AML patients with higher HOTAIR predicted worse clinical outcome compared with those with lower HOTAIR. Importantly, HOTAIR knockdown by small hairpin RNA inhibited cell growth, induced apoptosis, and decreased number of colony formation. Finally, HOTAIR modulated c-KIT expression by competitively binding miR-193a. Collectively, our data suggest that HOTAIR plays an important oncogenic role in AML and might serve as a marker for AML prognosis and a potential target for therapeutic intervention.

摘要

HOTAIR在多种癌症中显著过表达,并促进肿瘤侵袭和转移。然而,HOTAIR在急性髓系白血病(AML)中是否发挥致癌作用仍不清楚。在此,我们报告HOTAIR在白血病细胞系和原发性AML原始细胞中表达明显增加。临床上,与HOTAIR水平较低的AML患者相比,HOTAIR水平较高的患者临床预后更差。重要的是,通过小发夹RNA敲低HOTAIR可抑制细胞生长、诱导细胞凋亡并减少集落形成数量。最后,HOTAIR通过竞争性结合miR-193a调节c-KIT表达。总体而言,我们的数据表明HOTAIR在AML中发挥重要的致癌作用,可能作为AML预后的标志物和治疗干预的潜在靶点。

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