Fig. 4
From: FLIPL is critical for aerobic glycolysis in hepatocellular carcinoma
FLIPL promotes low glucose tolerance in HCC cells. a FACS analysis was performed to determine the apoptosis of HepG2, MHCC97-H, Huh-7, SMMC-7721 and BEL-7704 cells under low glucose (0.75 mM) or normal glucose (25 mM) treatment. b Immunoblot was used to detect the FLIPL and SGLT1 expression in MHCC97-H, HepG2, Huh-7, BEL-7704, and SMMC-7721 cell lines. c, d HepG2 cells were transfected with shSGLT1 vector. Expression was detected 48 h after transfection at protein and mRNA levels. **p < 0.01 versus control. e The apoptosis was measured in HepG2 cell with FLIPL knockdown treatment. Cells were cultured in low glucose (0.75 mM) or normal glucose (25 mM) and the levels of apoptosis were determined by FACS analysis. f Apoptosis was measured in HepG2 cell with SGLT1 knockdown. Cells were cultured in low glucose (0.75 mM) or normal glucose (25 mM), apoptosis was determined by FACS analysis. g Glucose uptake was measured in HepG2 cell with FLIPL knockdown or FLIPL knockdown plus SGLT1 overexpression treatment. h, i FLIPL-deficient HepG2 cells were transfected with the SGLT1 overexpression vector. Expression was detected 48 h after transfection at protein and mRNA levels. **p < 0.01 versus control. j Apoptosis was measured in HepG2 cell with FLIPL knockdown, SGLT1 knockdown, and FLIPL knockdown plus SGLT1 overexpression treatment. k Cell proliferation was measured by CCK8 assay in HepG2 cells with FLIPL knockdown, SGLT1 knockdown, and FLIPL knockdown plus SGLT1 overexpression treatment. (a, e, and f) Data represent the mean ± S.E.M. from three independent experiments, each performed in quadruplicate. **p < 0.01 versus 25 mM glucose group. (g, i, j, and k) Data represent the mean ± S.E.M. from three independent experiments, each performed in quadruplicate. *p < 0.05, **p < 0.01 versus control group; # p < 0.05 versus shFLIPL group