Skip to main content
Fig. 2 | Molecular Cancer

Fig. 2

From: Long non-coding RNA NEAT1-modulated abnormal lipolysis via ATGL drives hepatocellular carcinoma proliferation

Fig. 2

ATGL promotes HCC cell growth by maintaining elevated levels of DAG and FFA in vitro and in vivo. a Growth curves for the indicated HCC cells were evaluated by the Trypan blue dye exclusion method (left panel). CCK-8 assays showed that overexpression of ATGL promoted the growth of Huh7 cells (right panels). b Representative images of the cloning formation assay showed that overexpression of ATGL promoted the growth of Huh7 cells. c Growth curves for the indicated HCC cells were evaluated by the Trypan blue dye exclusion method (left panel). CCK-8 assays showed that sh-ATGL significantly inhibited HCC cell growth, however, this effect was completely rescued by treatment with 16 μM DAG+FFA (right panel). d Representative images of the cloning formation assay· showed that sh-ATGL significantly inhibited HCC cell growth and this effect was completely rescued by treatment with 16 μM DAG +FFA. e Representative bioluminescence imaging of Huh7 orthotopic HCC tumors f Volume of Huh-7 orthotopic tumors was determined at different timepoints. g The ratio of liver weight/body weight. h Representative images of immunohistochemical detection of Ki-67 in orthotopic HCC tissues. i Representative bioluminescence imaging of HCCLM3 orthotopic HCC tumors. j Volume of HCCLM3 orthotopic tumors was determined at different timepoints. k The ratio of liver weight/body weight. l Representative images of immunohistochemical detection of Ki-67 in orthotopic HCC tissues. m Relative levels of DAG and FFA was determined in 100 mg orthotopic HCC tissues. Two-way ANOVA with the Bonferroni’s correction was used in different timepoints statistical analysis. Data are expressed as mean ± SD of three independent experiments. Statistical significance was concluded at *P < 0.05, **P < 0.01, ***P < 0.001

Back to article page