Autocrine @entity650 -induced XXXX activation contributes to the pathogenesis of lung adenocarcinoma and @entity3483 .

@entity1 @entity650 @entity712 @entity7 @entity5 @entity4104 @entity19 @entity1149 @entity2 @entity3 @entity3483
@entity3483 ( @entity3483 ) is a poor prognostic sign for @entity1 with @entity1149 ( @entity1149 ). The generation of @entity3483 is largely regulated by @entity7 ( @entity7 ), and upregulation of @entity7 by @entity4104 has been observed in several types of @entity5 cells. In this study, we demonstrate constitutively activated @entity4104 in several @entity1 @entity2 cell lines and in @entity5 cells infiltrated in the pleurae of @entity1 with @entity2 ( @entity2 ) and @entity3483 . The observations suggest that activated @entity4104 plays a role in the pathogenesis of @entity2 . In PC14PE6/AS2 cells, a @entity4104 -positive @entity1 @entity2 cell line, autocrine @entity650 activated @entity4104 via JAKs, not via @entity19 kinase. PC14PE6/AS2 cells express higher @entity7 mRNA and protein than do @entity4104 -negative PC14PE6/AS2/dnStat3 cells. In an animal model, PC14P6/AS2/dnStat3 cells produced no @entity3483 and less lung @entity3 than did PC14P6/AS2 cells. PC14PE6/AS2 cells also expressed higher @entity7 protein, microvessel density, and vascular permeability in @entity5 than did PC14P6/AS2/dnStat3 cells. Therefore, we hypothesize that autocrine @entity650 activation of @entity4104 in @entity2 may be involved in the formation of @entity3483 by upregulating @entity7 . Higher levels of @entity650 and @entity7 were also found in the pleural fluids of @entity1 with @entity2 than in @entity1 with @entity712 . The autocrine @entity650 / @entity4104 / @entity7 signaling pathway may also be activated in @entity1 with @entity2 and @entity3483 . These findings provide novel targets for the management of @entity3483 .
