MicroRNA-196a post-transcriptionally upregulates the XXXX proto-oncogene and promotes cell proliferation in @entity0 .

@entity1 @entity0 @entity11216 @entity5 @entity32825
UNASSIGNED: Accumulating evidence has shown that @entity11216 -196a plays an important role in tumorigenesis and @entity5 progression in various types of @entity5 . miRNA profiling studies have suggested that @entity11216 -196a is highly overexpressed in @entity0 . However, the functional mechanism of @entity11216 -196a in @entity0 remains unclear. In the present study, we first showed that the expression of @entity11216 -196a was significantly upregulated in @entity1 @entity0 cell lines. Using a loss-of-function approach, we showed that the downregulation of @entity11216 -196a inhibited the proliferation of @entity0 cells in  vitro and in  vivo. @entity32825 ( @entity32825 ) gene as a cellular proto-oncogene, which was overexpressed and positively correlated with @entity11216  -196a expression in @entity0 tissues, was identified as a direct target of @entity11216 -196a. Moreover, in order to investigate whether @entity11216 -196a regulated cell growth in @entity0 cells by targeting @entity32825 , rescue studies were performed in @entity0 cells. The restoration of @entity32825 by transfecting @entity32825 cDNA in anti- @entity11216 -196a-tranfected @entity0 cells rescued the suppression of cell proliferation. In conclusion, the present study showed that @entity11216 -196a promoted cell proliferation by targeting @entity32825 in @entity0 . Thus, @entity11216 -196a may be a potential oncogene in @entity0 and a promising therapeutic target in @entity0 treatment.
