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. 2019 Oct 14;9(25):7599–7615. doi: 10.7150/thno.34931

Figure 4.

Figure 4

PGC-1β is critical for YY1-induced lipid accumulation in HCC cell. A. The protein expression levels of PGC-1β, MCAD and LCAD in YY1/PGC-1β-double silenced HepG2 (left) and MHCC-97H (right) cells, as examined using western blotting. B. The accumulation of lipid droplets in YY1/PGC-1β-double silenced HepG2 cells, as analyzed using Nile Red staining. Representative images (left) and relative fluorescence intensity (right, n = 9) are shown. C-D. The levels of cellular TG (C) and fatty acid β-oxidation (D) in YY1/PGC-1β-double silenced HepG2 (left) and MHCC-97H (right) cells (n = 3). E. Number of proliferative YY1/PGC-1β-double silenced HepG2 cells, as determined by EdU incorporation assay. Representative images (left) and ratio of the EdU positive cells to the total cell number (right) are shown (n = 9). All experiments were performed under hypoxic condition. Cells transfected with shCon were used as controls. β-actin was used as western blotting loading control. Quantification data are shown as mean ± SEM of three independent experiments. Scale bars: 200 μm. *P < 0.05; **P < 0.01 (ANOVA).