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

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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 chr14
start 49586580
end 49586878
lncRNA name 7SL
entrez id 6029
hgnc id HGNC:10038
ensg id ENSG00000276168
refseq id NR_002715
methods qPCR, Western blot, ChIP, Luciferase reporter assay etc.
regulated differential expression
function description In this study, we detected that over-expression of FOXP3 repressed the transcription of 7SL RNA and contributed to inhibiting tumor growth. Knock down of FOXP3 in MCF-10A normal mammary breast cells up-regulated the transcription of 7SL RNA. Chromatin Immuno-precipitation (ChIP) analysis showed that FOXP3 directly bound to the Forkhead/HNF-3 domain DNA binding sites (-789 to -795) relative to the transcription start site. Meanwhile, Luciferase analysis showed that FOXP3 repressed the full-length 7SL promoter activity, but this suppressive effect was reversed after mutation of the FOXP3 binding site. Further studies showed that FOXP3 promoted the expression of P53 at translational levels through repressing 7SL RNA.
pubmed id 26718402
year 2016
title Tumor FOXP3 represses the expression of long noncoding RNA 7SL.
drug X
circulating X
survival X

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