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

Figure 1.

Figure 1

YY1 induces hepatocellular carcinoma (HCC) cell lipid accumulation by regulating MCAD and LCAD expression. A-B. The accumulation of lipid droplets in YY1-silenced (A) and YY1-overexpressed (B) HepG2 cells, as determined using Nile Red staining. Representative images (left) and relative fluorescence intensity (right, n = 9) are shown. C. The accumulation of lipid droplets in YY1-silenced MHCC-97H cells, as examined using Nile Red staining. Representative images (left) and relative fluorescence intensity (right, n = 9) are shown. D-E. The levels of cellular triglyceride (TG) in YY1-silenced and YY1-overexpressed HepG2 (D) and MHCC-97H (E) cells (n = 3). F. mRNA expression levels of various lipid metabolic-associated factors in YY1-silenced HepG2 cells, as determined using quantitative reverse-transcribed PCR (qRT-PCR). Representative data are shown (n = 3). G-H. mRNA (G) and protein (H) expression levels of MCAD and LCAD in YY1-silenced HepG2 and MHCC-97H cells, as determined using qRT-PCR (n = 3) and western blotting, respectively. I. Protein expression levels of MCAD and LCAD in YY1-overexpressed HepG2 and MHCC-97H cells, as determined using western blotting. All experiments were performed under hypoxic condition. Cells transfected with shCon or pcCon were used as controls. β-actin was used for qRT-PCR normalization and as western blotting loading control. Scale bars: 200 μm. Quantification data are shown as mean ± SEM of three independent experiments. pcCon: pcDNA3.1(+); *P < 0.05; **P < 0.01; NS: not significant (ANOVA).