Journal
JOURNAL OF CELL BIOLOGY
Volume 210, Issue 4, Pages 613-627Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201501073
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Funding
- National Basic Research Program of China (973 Program) [2010CB529300]
- National Natural Science Foundation of China [81430072, 81120108005, 81225003, 81470805, 81270445, 81201929, 30900675, 81372609]
- Ministry of Science and Technology of China [2012AA02A504, 2015BAl13B07]
- China Scholarship Council [201306590015]
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MicroRNAs play essential roles in gene expression regulation during carcinogenesis. Here, we investigated the role of miR-7 and the mechanism by which it is dysregulated in gastric cancer (GC). We used genome-wide screenings and identified RELA and FOS as novel targets of miR-7. Overexpression of miR-7 repressed RELA and FOS expression and prevented GC cell proliferation and tumorigenesis. These effects were clinically relevant, as low miR-7 expression was correlated with high RELA and FOS expression and poor survival in GC patients. Intriguingly, we found that miR-7 indirectly regulated RELA activation by targeting the 10 kinase IKK epsilon. Furthermore, IKK epsilon and RELA can repress miR-7 transcription, which forms a feedback circuit between miR-7 and nuclear factor kappa B (NF-kappa B) signaling. Additionally, we demonstrate that down-regulation of miR-7 may occur as a result of the aberrant activation of NF-kappa B signaling by Heli-cobacter pylori infection. These findings suggest that miR-7 may serve as an important regulator in GC development and progression.
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