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Long noncoding  RNA s 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 ( PUM 1/ PUM 2). 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,  PUM 1 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.

Long noncoding RNA NORAD regulates transforming growth factor‐β signaling and epithelial‐to‐mesenchymal transition‐like phenotype