
HOTAIR , a prognostic factor in esophageal squamous cell carcinoma, inhibits WIF ‐1 expression and activates W nt pathway
Author(s) -
Ge XiaoSong,
Ma HuaJuan,
Zheng XiaoHui,
Ruan HongLian,
Liao XiaoYu,
Xue WenQiong,
Chen YuanBin,
Zhang Ying,
Jia WeiHua
Publication year - 2013
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.12296
Subject(s) - hotair , wnt signaling pathway , cancer research , long non coding rna , biology , epigenome , catenin , downregulation and upregulation , dna methylation , signal transduction , microbiology and biotechnology , gene expression , genetics , gene
Long non‐coding RNA s ( L nc RNA s) have been recently found to be pervasively transcribed in the genome and critical regulators of the epigenome. HOTAIR , as a well‐known L nc RNA , has been found to play important roles in several tumors. Herein, the clinical application value and biological functions of HOTAIR were focused and explored in esophageal squamous cell carcinoma ( ESCC ). It was found that there was a great upregulation of HOTAIR in ESCC compared to their adjacent normal esophageal tissues. Meanwhile, patients with high HOTAIR expression have a significantly poorer prognosis than those with low expression. Moreover, HOTAIR was further validated to promote migration and invasion of ESCC cells in vitro . Then some specific molecules with great significance were investigated after HOTAIR overexpression using microarray and quantitative real time‐polymerase chain reaction ( qPCR ). WIF ‐1 playing an important role in W nt/β‐catenin signaling pathway was selected and further tested by immunehistochemistry. Generally, inverse correlation between HOTAIR and WIF ‐1 expression was demonstrated both in ESCC cells and tissues. Mechanistically, HOTAIR directly decreased WIF ‐1 expression by promoting its histone H 3 K 27 methylation in the promoter region and then activated the W nt/β‐catenin signaling pathway. This newly identified HOTAIR / WIF ‐1 axis clarified the molecular mechanism of ESCC cell metastasis and represented a novel therapeutic target in patients with ESCC .