UHMK1 promotes gastric cancer progression through reprogramming nucleotide metabolism

A

SGC7901 and MGC803 cells were transfected with ATF4 shRNA or shcontrol. Western blottings and qRT–PCR were used to analyze the expression of UHMK1. Data were presented as mean ± standard deviation from three replicates. Unpaired two‐tailed statistical significance was assessed by Student's t‐test.

B

Overexpression of ATF4 enhanced the expression of UHMK1 in BGC823 and HGC27 cells. Data were presented as mean ± standard deviation from three replicates. Unpaired two‐tailed statistical significance was assessed by Student's t‐test.

C

The nucleotide sequences showing the −1,348/−948 region in the human UHMK1 gene. The red text indicates the candidate ATF4 binding sites.

D

The effect of ATF4 on the activity of the WT‐UHMK1 promoter and its mutations, as evaluated by using luciferase reporter assays.

E

ChIP assays were used to examine the binding of ATF4 to the UHMK1 promoter in SGC7901 and MGC803 cells. Input DNA and nonspecific IgG were included as controls.

F

ATF4 deficiency and overexpression regulated the activity of the UHMK1 promoter in GC cells.

Figure 7. ATF4 directly activates the transcription of the UHMK1 promoter in GC.