期刊
NUCLEIC ACIDS RESEARCH
卷 40, 期 9, 页码 3856-3869出版社
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkr1302
关键词
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资金
- Korea Research Foundation
- Korean Government (MOEHRD) [313-2008-2-C00876, 2009-0070260, 2010-0023905, BRL-2009-0087350]
- National Research Foundation of Korea (NRF) by the Ministry of Education, Science and Technology [2010-0029621]
- Ministry of Health Welfare [A101086]
- Ulsan University Hospital (Biomedical Research Center) [UUH-10-04]
- National Research Foundation of Korea [2010-0023905, 2009-0070260] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Tristetraprolin (TTP) is a AU-rich element (ARE) binding protein and exhibits suppressive effects on cell growth through down-regulation of ARE-containing oncogenes. The let-7 microRNA has emerged as a significant factor in tumor suppression. Both TTP and let-7 are often repressed in human cancers, thereby promoting oncogenesis by derepressing their target genes. In this work, an unexpected link between TTP and let-7 has been found in human cancer cells. TTP promotes an increase in expression of mature let-7, which leads to the inhibition of let-7 target gene CDC34 expression and suppresses cell growth. This event is associated with TTP-mediated inhibition of Lin28, which has emerged as a negative modulator of let-7. Lin28 mRNA contains ARE within its 3'-UTR and TTP enhances the decay of Lin28 mRNA through binding to its 3'-UTR. This suggests that the TTP-mediated down-regulation of Lin28 plays a key role in let-7 miRNA biogenesis in cancer cells.
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