Fig. 3: MRPL12 K163 acetylation inhibits ccRCC progression.
From: MRPL12 K163 acetylation inhibits ccRCC via driving mitochondrial metabolic reprogramming
A Wild-type (WT) MRPL12-HA and its K163R and K163Q mutants were transfected using lentivirus, and the acetylation of both WT and mutant MRPL12-HA proteins was detected with pan-acetylated lysine antibodies. B Wild-type (WT) MRPL12-HA and its K163R mutant were transfected using lentivirus, and the acetylation of both WT and mutant MRPL12-HA proteins was detected with acetylation site-specific antibodies. C Effects of transfecting the MRPL12 K163 mutant lentivirus on colony formation. D Effects of MRPL12 K163 mutant lentivirus transfection on wound healing in OS-RC-2 and 786-O cells. Scale bars: 200 μm. E Effects of MRPL12 K163 mutant lentivirus transfection on migration and invasion in OS-RC-2 and 786-O cells.Scale bars: 100 μm. F Effects of MRPL12 K163 mutant lentivirus transfection on EdU analyses. Scale bars: 100 μm. G Cell proliferation ability in OS-RC-2 and 786-O cells measured by Cell Counting Kit-8. H In vivo tumorigenesis in OS-RC-2 cells stably expressing wild-type or mutant MRPL12, assessed in a xenograft model (n = 5 mice per group). I Weights of xenograft tumors were analyzed (n = 5 mice per group). J Volumes of xenograft tumors were measured and analyzed (n = 5 mice per group). K IHC analysis on sections of xenograft tumors in nude mice to evaluate Ki-67 expression. Scale bars: 20 μm. Significance levels: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.
