The Genomic Atlas of Breast Cancer — the non-coding theme

Update News

  • GABC update 2020.06.15
  • GABC update 2019.03.20
  • GABC online 2018.08.09
  • Data collection 2018.04.09

About Us

  • Steven Xi Chen:
    steven.chen@miami.edu
  • Yunpeng Zhang:
    YXZ1418@med.miami.edu
  • Peng Wang:
    wpgqy@163.com
  • Shangwei Ning:
    ningsw@ems.hrbmu.edu.cn
  • Xia Li:
    lixia@hrbmu.edu.cn

Detail


Chr chr12
start 53962308
end 53974956
lncRNA name HOTAIR
entrez id 100124700
hgnc id HGNC:33510
ensg id ENSG00000228630
refseq id NR_003716
methods RC-PCR, Western blot, Luciferase reporter assay
regulated up-regulated
function description Paracrine TGF-B1 was essential for CAFs induced EMT and metastasis in breast cancer cells, which is a crucial mediator of the interaction between stromal and cancer cells. CAF-CM significantly enhanced the HOTAIR expression to promote EMT, whereas treatment with small-molecule inhibitors of TGF-B1 attenuated the activation of HOTAIR. Most importantly, SMAD2/3/4 directly bound the promoter site of HOTAIR, located between nucleotides -386 and -398, -440 and -452, suggesting that HOTAIR was a directly transcriptional target of SMAD2/3/4. Additionally, CAFs mediated EMT by targeting CDK5 signaling through H3K27 tri-methylation.
pubmed id 29325547
year 2018
title Paracrine and epigenetic control of CAF-induced metastasis: the role of HOTAIR stimulated by TGF-1 secretion.
drug X
circulating X
survival X

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