Fig. 6From: MiR-612 regulates invadopodia of hepatocellular carcinoma by HADHA-mediated lipid reprogrammingHADHA promotes β-oxidation of fatty acids in HCC. a OCR, the activities of β-oxidation, in HepG2 cells treated with 100 μM ETO, as well as in HepG2miR-612-KD, HepG2hadha-OE, and HepG2NC cells. b OCR, the activities of β-oxidation, in HCCLM3 cells treated with 100 μM ETO, as well as in HCCLM3miR-612-OE, HCCLM3hadha-KD, and HCCLM3NC cells. c The protein levels of Cortactin in HCCLM3 cells treated with 100 μM ETO or 100 mM linoleic acid, as well as in HCCLM3miR-612-o, HCCLM3miR-612-i, HCCLM3hadha-o, and HCCLM3hadha-i cells. d The intracellular levels of acetyl CoA in HCCLM3miR-612-o, HCCLM3hadha-i, and HCCLM3NC cells. e The cellular levels of cholesterol in HepG2miR-612-KD, HCCLM3miR-612-OE, HepG2hadha-OE, and HCCLM3hadha-KD cells. f The protein levels of Cortactin, Caveolin-1, E-cadherin, and GAPDH in HCCLM3 cells treated with or without 1 mM MβCD. g Fluorescence intensity in HepG2miR-612-i, HCCLM3miR-612-o, HepG2hadha-o, and HCCLM3hadha-i cells detected by fluorescence spectrophotometer (Ex/Em = 360/460 nm). Fluorescence polarization is calculated by the formula (h) The levels of ATP in HepG2miR-612-KD, HCCLM3miR-612-OE, HepG2hadha-OE, and HCCLM3hadha-KD cells analyzed by spectrophotometer (λ = 636 nm). (NS: no significance; *p < 0.05; **p < 0.01; ***p < 0.001). Data are mean ± SEM of three independent experimentsBack to article page