Journal
CARCINOGENESIS
Volume 36, Issue 8, Pages 925-935Publisher
OXFORD UNIV PRESS
DOI: 10.1093/carcin/bgv068
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Funding
- National Natural Sciences Foundation of China [81071921, 81372325]
- National High Technology Research and Development Program of China (863 Program) [2011AA02A111]
- Natural Sciences Foundation of Hubei Province [2012FFB05905]
- Research Fund of Wuhan Public Health Bureau [WX11A03, WX14C13, WX14B10]
- Youth Foundation of Wuhan Central Hospital [YQ13B04, YQ13A08]
- Yellow Crane Talent Plan Foundation
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To determine the role of miR-25 in non-small cell lung cancer (NSCLC), we first detected miR-25 expression in clinical specimens and lung cancer cell lines by quantitative real-time polymerase chain reaction. The levels of miR-25 were elevated in the plasma of NSCLC patients and NSCLC cell lines. Transfection of A549 and 95-D cells with a miR-25 inhibitor resulted in reduced cell proliferation and enhanced apoptosis. Moreover, the modulator of apoptosis 1 (MOAP1) gene was identified as a novel target of miR-25. The ability of miR-25 to promote cell proliferation and block apoptosis is attributable to its effect on MOAP1 suppression. In addition, miR-25 antagomir significantly inhibited lung cancer growth via upregulation of MOAP1 in a mouse xenograft model. Collectively, these data demonstrate that miR-25 is an important biomarker for lung cancer, and miR-25 promotes cell proliferation and inhibits apoptosis in NSCLC cells by negatively regulating MOAP1 expression.
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