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Long noncoding RNA NORAD regulates transforming growth factor‐β signaling and epithelial‐to‐mesenchymal transition‐like phenotype
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Long noncoding RNA NORAD regulates transforming growth factor‐β signaling and epithelial‐to‐mesenchymal transition‐like phenotype
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Journal Article
Long noncoding RNA NORAD regulates transforming growth factor‐β signaling and epithelial‐to‐mesenchymal transition‐like phenotype
2018
Overview
Long noncoding RNAs are involved in a variety of cellular functions. In particular, an increasing number of studies have revealed the functions of long noncoding RNA in various cancers; however, their precise roles and mechanisms of action remain to be elucidated. NORAD, a cytoplasmic long noncoding RNA, is upregulated by irradiation and functions as a potential oncogenic factor by binding and inhibiting Pumilio proteins (PUM1/PUM2). Here, we show that NORAD upregulates transforming growth factor‐β (TGF‐β) signaling and regulates TGF‐β‐induced epithelial‐to‐mesenchymal transition (EMT)‐like phenotype, which is a critical step in the progression of lung adenocarcinoma, A549 cells. However, PUM1 does not appear to be involved in this process. We thus focused on importin β1 as a binding partner of NORAD and found that knockdown of NORAD partially inhibits the physical interaction of importin β1 with Smad3, inhibiting the nuclear accumulation of Smad complexes in response to TGF‐β. Our findings may provide a new mechanism underlying the function of NORAD in cancer cells. We here show that lncRNA NORAD upregulates transforming growth factor‐β signaling and regulates EMT‐like phenotype in A549 lung adenocarcinoma cells. The identified function of NORAD is mediated by enhancement of nuclear translocation of Smad3 through binding to importin β 1, independent of the known molecular mechanism involving Pulmilio proteins.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
/ Carcinoma, Non-Small-Cell Lung - pathology
/ Epithelial-Mesenchymal Transition - physiology
/ epithelial‐to‐mesenchymal transition
/ Gene Expression Regulation, Neoplastic - physiology
/ Humans
/ Kinases
/ Motility
/ Original
/ Plasmids
/ Proteins
/ RNA
/ RNA, Long Noncoding - metabolism
/ Roles
/ Studies
/ Transforming Growth Factor beta1 - metabolism
