@entity44426 inhibited XXXX -induced epithelial-mesenchymal transition of @entity2 cells by inactivating of @entity125 signaling and switching on @entity27164 .

@entity44426 @entity4245 @entity5 @entity1135 @entity2 @entity5962 @entity189 @entity125 @entity519 @entity2277 @entity27164 @entity21507 @entity361 @entity8945 @entity6076 @entity72976 @entity62403
@entity361 ( @entity361 ) is an early step in the process of @entity5 metastasis. It is well known that @entity5 microenvironment affects @entity189 ; in particular, that @entity519 induces @entity361 . Deregulated notch signaling also contributes a lot to the development of @entity2 . In this study, we investigated the use of @entity125 -inhibiting compound as novel therapeutic candidates to regulate @entity519 -induced @entity2 cells. According to previous screening, @entity44426 was selected as a @entity125 inhibitor. @entity519 -induced @entity361 was characteristic of increased @entity6076 _ @entity2277 expressions and decreased @entity5962 expressions. Treatment with @entity44426 notably attenuated @entity519 -induced @entity361 , invasion and migration in H1299 cells, accompanied with reduced @entity125 , @entity72976 expressions and its downstream genes @entity21507 and @entity1135 . @entity44426 treatment also promoted tumorsuppressive @entity27164 level. Moreover, @entity125 siRNA prevented @entity519 -mediated cell migration and decreased @entity8945 , @entity4245 , and @entity62403 expressions, which are key @entity361 markers. Re-expression of @entity27164 blocked @entity519 -induced @entity361 and cell invasion. Our findings suggest that downregulation of @entity125 and reexpression of @entity27164 by @entity44426 might be a novel remedy for the therapy of @entity2 .
