Targeting glycolysis by XXXX improves @entity440 cytotoxicity of @entity0 cell lines.

@entity1 @entity35802 @entity0 @entity896 @entity440 @entity5 @entity19 @entity2041 @entity1234 @entity519 @entity3
BACKGROUND: @entity440 is the standard endocrine therapy for ER+ @entity0 ; however, many @entity1 still relapse after long-term therapy. @entity896 , a glycolytic inhibitor, has shown high selective anti- @entity5 activity in vitro, and in vivo. The aim of this study was to evaluate the possible augmentation of the effect of @entity440 via reprograming @entity5 cell metabolism using @entity896 . METHODS: An in vitro screening of antitumor activity as well as the apoptotic, anti-metastatic, and anti-angiogenic potentials of the combination therapy were carried out using different techniques on @entity0 cell lines MCF7and T47D. In addition the antitumor effect of the combined therapy was done on @entity19 @entity5 . RESULTS: Our results showed modulation in apoptosis, angiogenesis and metastatic potential by either drug alone; however, their combination has surpassed that of the individual one. Combination regimen enhanced activated @entity35802 , as well as oxidative stress, signified by increased @entity1234 and decreased @entity2041 level. Additionally, the angiogenesis and @entity3 markers, including @entity519 inducing factor-1a, vascular endothelia growth factor, and metaloproteinases-2 and 9 were decreased after using the combination regimen. These results were further confirmed by the in vivo study, which depicted a decrease in the @entity5 volume and angiogenesis and an increase in oxidative stress as well. CONCLUSION: @entity896 could be a valuable compound when added with @entity440 in @entity0 treatment.
