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- W2915479218 abstract "The tp53-induced glycolysis and apoptosis regulator (TIGAR) protein controls fructose-2, 6- bisphosphate (Fru-2, 6-P2) levels during glucose metabolism and helps maintain nicotinamide adenine dinucleotide phosphate (NADPH) levels to recycle glutathione (GSH), a key intracellular antioxidant. The present study was designed to investigate the apoptosis and autophagy mechanisms via reactive oxygen species (ROS) that underlie TIGAR knockdown in the A549 cell line. To detect the influence of siRNA-TIGAR on A549 lung cancer cells, we performed cell viabilty, colony formation, ROS, and NADPH assays. In addition, Western blotting and real-time polymerase chain reaction (PCR) assays were used to measure protein and mRNA expression levels, respectively. After TIGAR knockdown in A549 cell lines, various assay parameters were analyzed and showed that down-regulation of TIGAR inhibited viability and decreased colony formation. We also demonstrated that TIGAR knockdown induced apoptosis and autophagy, followed by an induction of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and heme oxygenase-1 (HO-1) expression. Furthermore, increased ROS levels and decreased NADPH levels were observed. This study supports our understanding of the possibility of employing TIGAR knockdown in lung cancer cells to enhance apoptosis and autophagy with NF-κB and HO-1 expression and then suggest TIGAR as a potential target for the treatment of lung cancer." @default.
- W2915479218 created "2019-03-02" @default.
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- W2915479218 date "2019-03-01" @default.
- W2915479218 modified "2023-10-14" @default.
- W2915479218 title "Knockdown of TIGAR Induces Apoptosis and Autophagy with Modulates NF-κB and HO-1 Expression in A549 Lung Cancer Cells" @default.
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- W2915479218 doi "https://doi.org/10.21597/jist.446068" @default.
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