Fig. 4: CENPT promoted RCC tumor proliferation and metastasis by increasing GSH synthesis in vitro and in vivo.
From: CENPT prevents renal cell carcinoma against ferroptosis by enhancing the synthesis of glutathione
A The interaction between CENPT and GCLC proteins was detected by co-immunoprecipitation assay. B, C Protein levels of GCLC in RCC cells after CENPT overexpression. D CENPT/GCLC interaction by GST-affinity pull-down assay. GST-CENPT was captured by glutathione-resin to probe the presence of HIS-GCLC with western blotting. E mRNA levels of GCLC in RCC cells after CENPT overexpression. F, G The catalytic activity of GCL in RCC cells after CENPT overexpression or knockdown. H–K The proliferation of RCC cells was detected by CCK8 and colony formation assay after co-transfection of shCENPT with GCLC overexpression. L–O Transwell assay suggested that GCLC overexpression reversed the inhibitory effect of knockdown of CENPT on migration and invasion. P, Q Intracellular ROS and lipid peroxidation level in different RCC cells. R Electron microscopy of RCCC cells after GCLC interaction with CENPT. Red arrows indicate damage to the mitochondrial membrane, increased or decreased membrane density, etc. R–X The in vivo effect of GCLC overexpression on shCENPT-mediated anti-RCC tumor growth. S, V Gross image of subcutaneous tumors. T, W Tumor growth curve of different groups. U, X The tumor weights of different groups. Data are given as mean ± SEM (in vitro assays, n = 3; in vivo assays, n = 5). Compared with the indicated group, *p < 0.05, **p < 0.01, ***p < 0.001.
