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 chr18
start 57054558
end 57072119
lncRNA name linc-ROR
entrez id 100885779
hgnc id HGNC:43773
ensg id ENSG00000258609
refseq id NR_048536
methods qPCR, Western blot, RIP etc.
regulated up-regulated
function description linc-RoR functions as an onco-lncRNA to promote estrogen-independent growth of ER+ breast cancer. Under estrogen deprivation, linc-RoR causes the upregulation of phosphorylated MAPK/ERK pathway which in turn activates ER signaling. Knockout of linc-RoR abrogates estrogen deprivation-induced ERK activation as well as ER phosphorylation, whereas re-expression of linc-RoR restores all above phenotypes. Moreover, we show that the ERK-specific phosphatase Dual Specificity Phosphatase 7 (DUSP7), also known as MKP-X, is involved in linc-RoR KOinduced repression of MAPK/ERK signaling. Interestingly, linc-RoR KO increases the protein stability of DUSP7, resulting in repression of ERK phosphorylation. Clinical data analysis reveal that DUSP7 expression is lower in ER+ breast cancer samples than that in ER- breast cancer. Moreover, downregulation of DUSP7 expression is associated with poor patient survival.
pubmed id 29041978
year 2017
title Linc-RoR promotes MAPK/ERK signaling and confers estrogen-independent growth of breast cancer
drug X
circulating X
survival V

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