XXXX -mediated chemo-resistance in @entity2 cells.

@entity7242 @entity3308 @entity5 @entity1149 @entity2 @entity1311 @entity4045 @entity584 @entity3546 @entity2355 @entity4975
@entity1311 ( @entity4045 ) is a commonly used drug to treat diverse @entity5 types. However, its treatment can generate resistance and the mechanisms of @entity4045 -resistance in @entity2 are still unclear. We demonstrated that @entity1149 ( @entity1149 ) survive @entity4045 treatment. Compared with the progenitor NSCLC A549 cells, the @entity4045 -resistant A549 cells (A549/ @entity4045 ) displayed enhanced sphere-formation ability. The proportion of the @entity5 stem cell marker, @entity4975 dehydrogenase-positive cells, and epithelial-mesenchymal transition signaling protein levels were also elevated in A549/ @entity4045 . Importantly, the levels of oncoproteins phosphoinositide-3 kinase/ @entity584 , @entity2355 cytoplasmic domain ( @entity2355 -C) and @entity3546 were also significantly elevated in A549/ @entity4045 . Furthermore, nuclear translocation of @entity2355 -C and @entity3546 increased in A549/ @entity4045 . The @entity7242 protein, an activator of @entity2355 -C, was also overexpressed in A549/ @entity4045 . These observations led to the hypothesis that enhanced expression of @entity2355 -C is associated with @entity3308 and @entity4045 resistance in @entity1149 . To test this, we knocked down or overexpressed @entity2355 -C in A549/ @entity4045 and found that inhibition of @entity2355 -C expression coupled with @entity4045 treatment was sufficient to reduce the sphere-forming ability and survival of A549/ @entity4045 . In summary, our in vitro and in vivo studies have revealed a potential mechanism of @entity2355 -C-mediated @entity4045 resistance and provided insights into a novel therapeutic measure for @entity2 .
