Fig. 6: GSH reversed the inhibitory effects of shCENPT on the growth, migration, and invasion of RCC.
From: CENPT prevents renal cell carcinoma against ferroptosis by enhancing the synthesis of glutathione
A The level of intracellular GSH content increased after overexpression of CENPT. B, C Intracellular GSH levels decreased after CENPT inhibition, which was reversed by overexpression of GCLC. D–G The expression of CENPT affects the expression level of GSH in vivo. H, I GSH increased protein expression levels of CENPT and GCLC in different cell lines. J mRNA Expression of CENPT in RCC cells after GSH treatment. K, L Co-IP assays demonstrated the direct binding between GSH and ATF2. M The predicted binding sites of ATF2 to the promoter of CENPT. N ChIP-PCR experiments demonstrated direct binding of ATF2 to the promoter regions of CENPT in RCC cells. O The luciferase reporter gene assay was used to determine the ATF2 binding sites on the CENPT promoter region. P Following GSH treatment, the CCK-8 assay was employed to determine the growth curve of shCENPT-treated RCC cells. Q, R Colony formation assays were conducted to assess the proliferative capacity of shCENPT-treated RCC cells under the influence of GSH. S, T The EdU incorporation assay was utilized to detect the proliferation status of different RCC cells after GSH treatment. Data are given as mean ± SEM (n = 3). Compared with the indicated groups, *p < 0.05, **p < 0.01, ***p < 0.001.
