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Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
07:49

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

11.8K

Long noncoding RNA NORAD regulates transforming growth factor-β signaling and epithelial-to-mesenchymal

Natsumi Kawasaki1, Toshiki Miwa1, Satoshi Hokari1,2

  • 1Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Cancer Science
|May 4, 2018
PubMed

Insights

Long noncoding RNA NORAD promotes lung adenocarcinoma by upregulating transforming growth factor-β (TGF-β) signaling. NORAD influences TGF-β-induced epithelial-to-mesenchymal transition via importin β1, not Pumilio proteins.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Long noncoding RNAs (lncRNAs) play diverse cellular roles, with emerging evidence highlighting their involvement in cancer.
  • NORAD, a lncRNA, is implicated as an oncogenic factor, potentially by inhibiting Pumilio proteins (PUM1/PUM2).

Purpose of the Study:

  • To elucidate the precise roles and mechanisms of NORAD in lung adenocarcinoma progression.
  • To investigate NORAD's regulation of transforming growth factor-β (TGF-β) signaling and associated cellular phenotypes.

Main Methods:

  • Investigated NORAD's effect on TGF-β signaling and epithelial-to-mesenchymal transition (EMT)-like phenotype in A549 lung adenocarcinoma cells.
  • Examined the interaction of NORAD with Pumilio proteins (PUM1/PUM2) and importin β1.
  • Assessed the impact of NORAD knockdown on importin β1 and Smad3 interaction and nuclear accumulation.

Main Results:

  • NORAD upregulates TGF-β signaling and promotes a TGF-β-induced EMT-like phenotype in lung adenocarcinoma cells.
  • Pumilio proteins (PUM1/PUM2) were not found to be involved in this NORAD-mediated process.
  • NORAD knockdown partially inhibits the interaction between importin β1 and Smad3, thereby reducing Smad complex nuclear accumulation in response to TGF-β.

Conclusions:

  • NORAD functions as an oncogenic factor in lung adenocarcinoma by modulating TGF-β signaling.
  • The mechanism involves NORAD's interaction with importin β1, influencing Smad3 nuclear translocation, rather than Pumilio proteins.
  • These findings reveal a novel mechanism for NORAD's function in cancer cells.
Keywords:
epithelial-to-mesenchymal transitionlong noncoding RNAnon-small-cell lung cancernuclear transporttransforming growth factor-β

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