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 chr20
start 57710183
end 57712780
lncRNA name NKILA
entrez id 105416157
hgnc id HGNC:51599
ensg id ENSG00000278709
refseq id NR_131157
methods qPCR, Western blot etc.
regulated up-regulated
function description In this study, we found that TGF-B activates the NF-kB pathway. Inhibition of NF-kB signaling markedly abrogates TGF-B-induced EMT. By studying the regulatory mechanism of TGF-B-induced NF-kB signaling, we found that lncRNA NKILA was upregulated by TGF-B and was essential for the negative feedback regulation of the NF-kB pathway. Accordingly, overexpression of NKILA significantly reduced TGF-B-induced tumor metastasis in vivo. Consistent with the results from mice, the expression of NKILA was negatively correlated with EMT phenotypes in clinical breast cancer samples. Collectively, our study findings indicated that the NKILA-mediated negative feedback affects TGF-B-induced NF-kB activation and that NKILA may be a therapeutic molecule in breast cancer metastasis via inhibition of EMT.
pubmed id 29761481
year 2018
title LncRNA NKILA Suppresses TGF-B-induced Epithelial-Mesenchymal Transition by Blocking NF-kB Signaling in Breast Cancer.
drug X
circulating X
survival V

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