Targeting protein @entity369 methyltransferase 5 inhibits @entity14 growth by decreasing @entity369 methylation of XXXX and @entity2557 .

@entity1 @entity1380 @entity5 @entity19 @entity2557 @entity71130 @entity14 @entity1379 @entity4043 @entity369
UNASSIGNED: Protein @entity369 methyltransferases (PRMTs) plays critical roles in @entity5 . @entity71130 has been implicated in several types of @entity5 . However, the role of @entity71130 in @entity5 development remains to be fully elucidated. Here, we provide evidence that @entity71130 is overexpressed in @entity14 ( @entity14 ) cells and @entity1 -derived @entity5 , correlated with increased cell growth and decreased overall @entity1 survival. @entity369 methyltransferase inhibitor 1 (AMI-1)strongly inhibited @entity5 growth, increased the ratio of @entity1380 / @entity1379 , and induced apoptosis in @entity19 @entity14 xenograt model. AMI-1 also induced apoptosis and decreased the migratory activity in several @entity14 cells. In @entity14 xenografts AMI-1 significantly decreased symmetric dimethylation of histone 4 (H4R3me2s), a histone mark of type II @entity71130 , but not the expression of H4R3me2a, a histone mark of type I PRMTs. These results suggest that the inhibition of @entity71130 contributes to the antitumor efficacy of AMI-1. Chromatin immunoprecipitation (ChIP) identified @entity2557 and @entity4043 as two key genes regulated by @entity71130 . @entity71130 knockdown reduced the levels of H4R3me2s and H3R8me2s methylation on @entity2557 and @entity4043 promoters, leading to decreased expressions of @entity2557 and @entity4043 . Collectively, our findings provide new evidence that @entity71130 plays an important role in @entity14 pathogenesis through epigenetically regulating @entity369 methylation of oncogenes such as @entity4043 and @entity2557 .
