Our previous study has showed that @entity21158 acts as a  functional @entity5 suppressor in @entity14 ( @entity14 ) cell lines. The aims of this study were to determine whether @entity21158 is a  target of MicroRNA (miRNA) regulation and to evaluate the role of this mechanism in @entity14 . By bioinformatics approach and literature, @entity18842 was chosen for further study. The @entity18842 mimic, @entity18842 inhibitor were synthesized and transfected to Lovo cells. Cell growth was determined by @entity98 and in vivo models. The flow cytometric analysis for cell cycle determination and transwell assays for evaluating the cell invasion were used. Luciferase reporter assays and Western blots showed that @entity21158 was a  direct target of @entity18842 in @entity14 . The expression levels of @entity18842 were obviously up-regulated in @entity14 tissues compared to non-cancerous tissues, while @entity21158 expression levels were down-regulated in a  high proportion of clinical samples (14/18). In addition, correlation analyses revealed negative correlation between @entity18842 levels and @entity21158 expression levels in @entity14 tissues. @entity18842 overexpression promoted cell growth in vitro and in vivo, promoted cell cycle progression and invasion in Lovo cells. Furthermore, re-introduction of @entity21158 in @entity18842 -overexpressing Lovo cells decreased growth rate of cells, increase of the percentage in G0/G1 phase and decreased the number of migrating cells. In conclusion, we demonstrated that @entity18842 is up-regulated in @entity14 and acts as a  functional oncogene by targeting @entity21158 .

MicroRNA-141 regulates the @entity5 suppressor XXXX in @entity14 .

@entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity21158 :: ('10395', 'Gene') :: ['DLC-1', 'DLC1'] @entity18842 :: ('406933', 'Gene') :: ['MiR-141', 'miR-141'] @entity98 :: ('CHEBI:53233', 'Chemical') :: ['MTT'] @entity14 :: ('MESH:D015179', 'Disease') :: ['CRC', 'colorectal cancer']
@entity21158 :: (10395,Gene) :: ['DLC1']
