HOTAIR regulates HK2 expression by binding endogenous miR-125 and miR-143 in oesophageal squamous cell carcinoma progression.
HOTAIR regulates HK2 expression by binding endogenous miR-125 and miR-143 in oesophageal squamous cell carcinoma progression.
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HOTAIR 通过结合内源性 miR-125 和 miR-143 在食管鳞状细胞癌进展中调节 HK2 表达
DOI:
10.18632/oncotarget.21195
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发表时间:
2017-10-17
期刊:
影响因子:
--
通讯作者:
Cao X
中科院分区:
文献类型:
--
作者:
Ma J;Fan Y;Feng T;Chen F;Xu Z;Li S;Lin Q;He X;Shi W;Liu Y;Liu Z;Zhu B;Cao X
Esophageal Squamous Cell Carcinoma (ESCC) is one of the most common malignant cancers worldwide with a high death rate worldwide. Long non-coding RNA (LncRNA) has been recently demonstrated to play a critical role in ESCC. LncRNA HOTAIR played important regulatory roles in ESCC. We highlight the molecular mechanisms by which HOTAIR could influence the expression of Hexokinase 2 (HK2) in ESCC through binding miR-125 and miR-143 directly. Taken together, this study identified a functional lncRNA HOTAIR involved with regulation of glycolysis via miRNA-125/miRNA-143-HK2 in ESCC cells. The “competitive endogenous RNA” (ceRNA) model of HOTAIR/miR-125 and miR143/HK2 interaction might serve as important targets for ESCC diagnosis and therapy.