HOTAIR regulates HK2 expression by binding endogenous miR-125 and miR-143 in oesophageal squamous cell carcinoma progression

HOTAIR通过结合内源性miR-125和miR-143调控HK2表达,从而参与食管鳞状细胞癌的进展。

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Abstract

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.

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