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Fig. 4 | Journal of Translational Medicine

Fig. 4

From: Long noncoding RNA lncARSR promotes nonalcoholic fatty liver disease and hepatocellular carcinoma by promoting YAP1 and activating the IRS2/AKT pathway

Fig. 4

LncARSR increases cell proliferation, invasion, and cycle as well as lipid accumulation in oleate-treated HepG2 cells. Oleate-treated HepG2 cells were infected with lentivirus of sh-lncARSR, sh-NC, oe-lncARSR or oe-NC. a Expression of YAP1, IRS2, AKT and phosphorylation of AKT proteins in HepG2 cells. b Lipid accumulation in HepG2 cells (×400). c TG content in HepG2 cells. d Expression of adipogenesis related proteins (Fasn, Scd1 and GPA) and PPARγ in HepG2 cells. e Cell proliferation determined by MTT assay. f Cell proliferation monitored by soft-agar colony formation. g Cell cycle examined by flow cytometry. h Cell invasion inspected by transwell assay (× 200). *p < 0.05 against oleate-treated HepG2 cells treated with sh-NC; #p < 0.05 against oleate-treated HepG2 cells treated with oe-NC. Measurement data were expressed as mean ± standard deviation from at least three independent repeated experiments. Unpaired t-test and one-way ANOVA were used for comparisons between or among two groups or multiple groups

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