期刊
CANCER CELL
卷 27, 期 3, 页码 370-381出版社
CELL PRESS
DOI: 10.1016/j.ccell.2015.02.004
关键词
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资金
- 973 Projects from Ministry of Science and Technology of China [2011CB504203, SQ2015CB050449]
- Natural Science Foundation of China [81230060, 81490751, 8144000006, 8141101179, 81442009, 81302369, 81272894, 81472467, 81472466, 81372819, 81272893]
- Science Foundation of Guangdong Province [S2012030006287, 2014J4100170, 2012J2200092]
- Translational medicine public platform of Guangdong Province [4202037]
- Guangdong Department of Science & Technology Translational Medicine Center grant [2011A080300002]
- Program for New Century Excellent Talents [NCET-12-0565]
- Specialized Research Fund for the Doctoral Programof Higher Education [20120171110075]
- Fundamental Research Funds for the Central Universities [13ykpy27, 13ykzd14]
- Fund for Excellent Doctoral Dissertation of Guangdong Province [81000-3212502]
- Guangdong Provincial National Science Fund for Distinguished Young Scholars
- Elite Young Scholars Program of Sun Yat-sen Memorial Hospital [Y201401]
NF-kappa B is a critical link between inflammation and cancer, but whether long non-coding RNAs (lncRNAs) regulate its activation remains unknown. Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kappa B, binds to NF-kappa B/I kappa B, and directly masks phosphorylation motifs of I kappa B, thereby inhibiting IKK-induced I kappa B phosphorylation and NF-kappa B activation. Unlike DNA that is dissociated from NF-kappa B by I kappa B, NKILA interacts with NF-kappa B/I kappa B to form a stable complex. Importantly, NKILA is essential to prevent over-activation of NF-kappa B pathway in inflammation-stimulated breast epithelial cells. Furthermore, low NKILA expression is associated with breast cancer metastasis and poor patient prognosis. Therefore, lncRNAs can directly interact with functional domains of signaling proteins, serving as a class of NF-kappa B modulators to suppress cancer metastasis.
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