User:Dahle001

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Figure 2, part D

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Figure 1, part A2

Figure 1A: Protein and mRNA levels of ATF4 were determined using Western Blot and qPCR. β-actin and GAPDH were used as a control.

Figure 1B, C, D, E, H: When transfected into SGC7901 and AGS cells, colony number increased due to overexpression of ATF4. When ATF4 was knocked out of expression in SGC7901/ADR and SGC7901/VCR cells the colony number decreased. This shows that ATF4 produced multi-drug resistance in cancer cells, allowing for cell growth.

Figure 2: "The overexpression of ATF4 was associated with increased SIRT1 expression at both the transcriptional (Fig. 2A, left) and translational levels (Fig. 2B, left). In contrast, siRNA knockdown of ATF4 in SGC7901/ADR cells resulted in a significant reduction of endogenous SIRT1 expression (Fig. 2A and 2B, right). These results suggest that ATF4 up-regulates SIRT1 expression in gastric cancer cells."

Figure 3A and C: "The luciferase reporter assay showed that the SIRT1 promoter activity was markedly activated by ATF4 in a dose-dependent manner... Cells showed enrichment of both binding sites within the SIRT1 promoter region, indicating that the RNA and subsequent protein level increases of SIRT1 in ATF4-expressing cell lines are likely due to a direct interaction of ATF4 with the SIRT1 gene promoter"

Figure 4: Knockdown of SIRT1 allows the cells to become sensitive to the drug. Data shows that SIRT1 allows the cell to be drug resistant.

Figure 5A-C: overexpression of SIRT1 allows for the downregulation of apoptosis, allowing for ATF4-induced multi-drug resistance in gastric cancer.

Figure 6: These results suggest that SIRT1 activity also plays a critical role in the ATF4-induced gastric cancer MDR and this role might be mediated partly through MDR1 expression.

Figure 1: "The expression level of the gene is lower in almost all patients CVH-385-IV-13, CVH-385-IV-11, 07–0153 compared to control, suggesting nonsense mediated mRNA decay."

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"we also demonstrated that FAS is induced by insulin using freshly isolated human endothelial cells (Fig. 1B"

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