Fig. 6
LAT2 targets glutamine-dependent mTOR activation to regulate apoptosis, glycolysis and chemosensitivity in pancreatic cancer cells. a, b, d, e The percentage of apoptotic MIA PaCa-2 and PANC-1 cells with LAT2 OE was higher than the percentage of apoptotic control cells when the L-glutamine concentration was normal (4 mM); however, glutamine deprivation reversed the decrease in the percentage of apoptotic cells induced by LAT2; glutamine deprivation increased the percentage of apoptotic MIA PaCa-2 and PANC-1 cells. c, f Glutamine deprivation reversed the increase in ECAR and glycoPER induced by LAT2 in MIA PaCa-2 and PANC-1 cells; RAD001 decreased ECAR but not glycoPER in MIA PaCa-2 and PANC-1 cells, regardless of LAT2 expression level. g Exogenous L-glutamine activated the mTOR pathway and upregulated p-mTOR, p-4EBP1 and p21 in MIA PaCa-2 and PANC-1 cells. h Glutamine deprivation promoted the dissociation of LAT2 and p-mTORSer2448. i Glutamine deprivation in MIA PaCa-2 and PANC-1 cells reversed the mTOR activation induced by LAT2 OE. The data are presented as the mean ± SD. (Student’s t-test; *, P < 0.05)