Overexpression of the regulator of G-protein signaling  5 reduces the survival rate and enhances the radiation response of @entity1 XXXX cells.

@entity46337 @entity1 @entity9189 @entity51781 @entity589 @entity588 @entity5 @entity2 @entity5605 @entity876 @entity23759 @entity98 @entity9067 @entity9190 @entity563
UNASSIGNED: @entity51781 ( @entity51781 ) belongs to the R4 subfamily of @entity46337 proteins, a family of GTPase activating proteins, which is dynamically regulated in various biological processes including blood pressure regulation, smooth muscle cell pathology, fat metabolism and @entity5 angiogenesis. Low-expression of @entity51781 was reported to be associated with @entity5 progression in @entity2 . In the present study, we examined the potential roles of @entity51781 in @entity1 @entity2 cells by overexpressing @entity51781 in the @entity5 cells and further explored the underlying molecular mechanisms. The @entity51781 gene was cloned and transfected into the @entity1 @entity2 cell lines A549 and @entity1 . The cells were tested for apoptosis with flow cytometry, for viability with @entity98 , for mobility and adhesion capacity. The radiosensitization effect of @entity51781 was measured by a colony formation assay. The mechanisms of @entity51781 functioning was also investigated by detection of protein expression with western blot analysis, including @entity9190 , @entity9189 , @entity589 , @entity588 , @entity9067 , @entity23759 , @entity5605 , phospho- @entity876 ( @entity563  15) and @entity876 . The present study demonstrated that @entity51781 overexpression remarkably induced apoptosis in @entity1 @entity2 cells, which was suggested to be through mitochondrial mechanisms. Overexpression of @entity51781 resulted in significantly lower adhesion and migration abilities of the @entity2 cells (P<0.01). Furthermore, overexpression of @entity51781 sensitized the @entity2 cells to radiation. In conclusion, the present study showed that @entity51781 played an inhibitory role in @entity1 @entity2 cells through induction of apoptosis. Furthermore, @entity51781 enhanced the cytotoxic effect of radiation in the @entity1 @entity2 cells. Our results indicated that @entity51781 may be a potential target for @entity5 therapy.
