Fig. 4: HIF1α promotes DDIT4 expression to stimulate cell proliferation, invasion, and migration and inhibit apoptosis in NPC.

a RT-qPCR detection of DDIT4 mRNA expression in clinical NPC tissues and adjacent tissues. b Western blot analysis of DDIT4 protein expression in clinical NPC tissues and adjacent tissues. c Pearson analysis of the correlation between the expression of HIF1α and DDIT4. d RT-qPCR detection of DDIT4 mRNA silencing interference efficiency. e RT-qPCR detection of mRNA expression of HIF1α and DDIT4 in each group of cells. f Western blot analysis of HIF1α and DDIT4 protein expression in each group of cells. g MTT detection of cell proliferation in each group. h Transwell detection of cell migration ability in each group. i Transwell assay detection of the cell invasion ability of each group. j Flow cytometry detection of the apoptosis in each group. k Western blot analysis of the expression of cell proliferation (Ki67, cyclin D1), migration (MMP-2, MMP-9), and apoptosis (Bcl-2, Bax)-related factors in each group. *p < 0.05 vs. control cells, cells treated with si-D-NC or cells cotreated with OE-NC and si-D-NC, # p < 0.05 vs. cells cotreated with OE-NC and si-DDIT4. & p < 0.05 vs. cells cotreated with OE-HIF1α and si-D-NC. NS meant no significant difference. The measurement data are expressed as the mean ± standard deviation. Data between cancer tissues and adjacent tissues were compared using paired t tests. One-way ANOVA was used for multigroup comparisons. Cell viability at different time points was analyzed using two-way ANOVA. For patients, n = 55. The experiment was repeated three times independently.