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

•HOTAIR is upregulated in AML blasts.•HOTAIR facilitates proliferation.•HOTAIR modulates c-KIT.•High expression of HOTAIR predicts poor outcome. HOTAIR is significantly overexpressed in various cancers and facilitates tumor invasion and metastasis. However, whether HOTAIR plays oncogenic roles in ac...

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Bibliographic Details
Published in:	FEBS letters 2015-07, Vol.589 (15), p.1981-1987
Main Authors:	Xing, Chong-yun, Hu, Xiao-qu, Xie, Fei-yan, Yu, Zhi-jie, Li, Hai-ying, Bin-Zhou, Wu, Jian-bo, Tang, Li-yuan, Gao, Shen-meng
Format:	Article
Language:	eng
Subjects:	Acute myeloid leukemia c-KIT Cell Line, Tumor HOTAIR Humans Leukemia, Myeloid, Acute - genetics Leukemia, Myeloid, Acute - pathology Luciferases - genetics Luciferases - metabolism MicroRNAs - genetics MicroRNAs - physiology miR-193a Prognosis Proto-Oncogene Proteins c-kit - genetics Real-Time Polymerase Chain Reaction RNA, Long Noncoding - metabolism RNA, Long Noncoding - physiology Up-Regulation
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Summary:	•HOTAIR is upregulated in AML blasts.•HOTAIR facilitates proliferation.•HOTAIR modulates c-KIT.•High expression of HOTAIR predicts poor outcome. 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.
ISSN:	0014-5793 1873-3468