@entity2903 ( @entity2904 ) is widely used for @entity1 with @entity463 ( @entity463 ); however, @entity5 cells frequently exhibit drug-resistance. Base excision repair (BER) has been identified as a possible mediator of @entity2904 resistance, and an attractive approach to sensitizing cells to chemotherapy. @entity1 @entity6471 ( @entity6471 ) is an essential enzyme with a role in the BER pathway by repairing abasic sites, and it also acts as a reduction factor, maintaining transcription factors in an active reduced state. Thus, we aimed to investigate whether the down-regulation of @entity6471 expression by siRNA can interfere with the resistance of @entity463 to @entity2904 , being evaluated by several cellular and molecular parameters. We demonstrated that @entity6471 knockdown associated with @entity2904 treatment efficiently reduced cell proliferation and clonogenic survival of resistant cells (T98G), which appears to be a consequence of increased DNA damage, S-phase arrest, and @entity6714 phosphorylation, resulting in apoptosis induction. On the contrary, for those assays, the sensitization effects of @entity6471 silencing plus @entity2904 treatment did not occur in the @entity2904 -sensitive cell line (U87MG). Interestingly, @entity2904 -treatment and @entity6471 knockdown significantly reduced cell invasion in both cell lines, but @entity2904 alone did not reduce the invasion capacity of U87MG cells, as observed for T98G. We also found that @entity7 expression was down-regulated by @entity2904 treatment in T98G cells, regardless of @entity6471 knockdown, but U87MG showed a different response, since @entity6471 silencing counteracted @entity7 induction promoted by @entity2904 , suggesting that the @entity6471 -redox function may play an indirect role, depending on the cell line. The present results support the contribution of BER in the @entity463 resistance to @entity2904 , with a greater effect in @entity2904 -resistant, compared with @entity2904 -sensitive cells, emphasizing that @entity6471 can be a promising target for modifying @entity2904 tolerance. Furthermore, genetic characteristics of @entity5 cells should be considered as critical information to select an appropriate therapeutic strategy.

@entity6471 / @entity6471 down-regulation enhances the cytotoxic effects of @entity2903 in a resistant XXXX cell line.

@entity1 :: ('9606', 'Species') :: ['patients', 'Human'] @entity7 :: ('7422', 'Gene') :: ['VEGF'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity2904 :: ('CHEBI:72564', 'Chemical') :: ['TMZ'] @entity6471 :: ('328', 'Gene') :: ['APE1', 'apurinic/apyrimidinic endonuclease/redox factor-1'] @entity2903 :: ('MESH:C047246', 'Chemical') :: ['Temozolomide'] @entity463 :: ('MESH:D005909', 'Disease') :: ['GBM', 'glioblastoma'] @entity6714 :: ('3014', 'Gene') :: ['H2AX']
@entity463 :: (MESH:D005909,Disease) :: ['glioblastoma']
