Fig. 6: Deacetylation of K62 promotes cells proliferation in vivo and in vitro. | Cell Death & Disease

Fig. 6: Deacetylation of K62 promotes cells proliferation in vivo and in vitro.

From: HDAC8-dependent deacetylation of PKM2 directs nuclear localization and glycolysis to promote proliferation in hepatocellular carcinoma

Fig. 6

CCK-8 assay (A), colony formation (B), and immunofluorescence analysis with EdU (Scale bar: 20 μm) C were performed to evaluate the effect of HDAC8 knockout and the K62 acetylation deficiency on the proliferation ability of HepG2 cells. Data shown are mean ± SD (n = 3) (*P < 0.05, **P < 0.01, ***P < 0.001). D Image of xenograft tumors resected from tumor-bearing NCG mice (n = 4). E Representative 18F-FDG micro-PET/CT images of two living NCG mice were conducted 5 weeks after subcutaneous inoculation. Images showed the obvious different ability of FDG uptake in different groups of xenografts. F The tumor tissues were examined by hematoxylin and eosin(H/E), anti-ac-lys-62-PKM2 antibodies, HDAC8, Ki-67, Cyclin D1 and Glut1(scale bar, 100 μm). The analysis of the intensity of cyclin D1 expression by image J. (*P < 0.05, one way ANOVA in A, B, D, E, F).

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