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. 2024 Jul 30;15(7):541. doi: 10.1038/s41419-024-06933-x

Fig. 5. TKT mediates HMGA1-upregulated PPP.

Fig. 5

A–C Control and HMGA1-knocked down KYSE30 cells were transfected with Flag-tagged TKT. TKT enzyme activity (A), NADPH (B), and GSH (C) were determined in cells. D, E Enforced expression of TKT ameliorates HMGA1 depletion-induced DNA damage. Control and HMGA1-knocked down KYSE30 cells were transfected with pcDNA3.1/TKT for 24 h. Cells were then treated with 10 μm CDDP for another 16 h. After the treatment, cells were collected for determining the expression of γ-H2AX (Ser139), HMGA1, and TKT by western blotting (D) or subjected to the immunofluorescence staining for detecting the expression of γ-H2AX (Ser139) (E). Scale bar, 10 μm. F–H Control and HMGA1-overexpressed TE13 cells were transfected with TKT siRNA and detected for TKT enzyme activity (F), NADPH (G), and GSH (H). I, J Depletion of TKT reverses HMGA1-alleviated DNA damage. Control and HMGA1-overexpressed TE13 cells were transfected with TKT siRNA for 24 h. Cells were then treated with 10 μm CDDP for another 16 h. After the treatment, cells were used for determining the expression of γ-H2AX (Ser139), HMGA1, and TKT by western blotting (I) or fixed for the immunofluorescence detection of γ-H2AX (Ser139) (J). Scale bar, 5 μm.