Journal
CANCER SCIENCE
Volume 109, Issue 7, Pages 2211-2220Publisher
WILEY
DOI: 10.1111/cas.13626
Keywords
epithelial-to-mesenchymal transition; long noncoding RNA; non-small-cell lung cancer; nuclear transport; transforming growth factor-beta
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Funding
- Japan Society for the Promotion of Science (JSPS) [15K06831, 15H05774]
- Research on Development of New Drugs (Japan Agency for Medical Research and Development [AMED])
- Princess Takamatsu Cancer Research Fund
- Research Fellowship for Young Scientists
- Graduate Program for Leaders in Life Innovation from JSPS
- Grants-in-Aid for Scientific Research [15K06831] Funding Source: KAKEN
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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- (TGF-) signaling and regulates TGF--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 1 as a binding partner of NORAD and found that knockdown of NORAD partially inhibits the physical interaction of importin 1 with Smad3, inhibiting the nuclear accumulation of Smad complexes in response to TGF-. Our findings may provide a new mechanism underlying the function of NORAD in cancer cells.
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