Fig. 6: TIP60 involves in MRPL12 K163 Acetylation in ccRCC.
From: MRPL12 K163 acetylation inhibits ccRCC via driving mitochondrial metabolic reprogramming
A TIP60, PCAF, and P300 siRNA were transfected into HEK293T cells, and their knockdown efficiencies were assessed by Western blot (WB) analysis. B MRPL12 K163 acetylation levels in OS-RC-2 cells were analyzed following transfection with siRNA targeting TIP60, PCAF, and P300. C Endogenous interactions between MRPL12 and TIP60 in OS-RC-2 and 786-O cells were determined by immunoprecipitation (IP) and immunoblot (IB) analysis. D, E HEK293T cells were transfected with Flag-MRPL12 and Myc-TIP60 as indicated. Interactions between MRPL12 and TIP60 were assessed by co-IP and IB analysis. F AlphaFold 3 simulation illustrating the predicted interaction between MRPL12 and TIP60. G Interaction between MRPL12 and TIP60 in OS-RC-2 cells detected by Duolink proximity ligation assay. Scale bar: 10 μm, n = 3 per group. H Silencing TIP60 decreased endogenous K163 acetylation of MRPL12. I TIP60 overexpression increased endogenous K163 acetylation of MRPL12. J Effect of TIP60 knockdown and overexpression on cell migration. Scale bar: 100 μm. K Regulation of TIP60/KAT5 expression across various tumor types as shown in The Cancer Genome Atlas (TCGA) Database. L Comparison of TIP60/KAT5 expression between ccRCC tissues and normal tissue (NTL), showing reduced expression in ccRCC from the UALCAN database. M Significant correlation between TIP60/KAT5 expression and ccRCC staging identified in the UALCAN database. N Survival analysis evaluating overall survival of ccRCC patients, conducted using the GEPIA and Xiantao databases. Significance levels: ns, P > 0.05; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
