Fig. 3

LAT2 activates glycolysis in pancreatic cancer cells and alters glutamine metabolism to activate mTOR in vitro and in vivo. a, b LAT2 knockdown significantly decreased ECAR and OCR in MIA PaCa-2 and PANC-1 cells and promoted the transformation of cell metabolic phenotype from an energetic to a quiescent phenotype; LAT2 overexpression significantly increased ECAR and OCR in MIA PaCa-2 and PANC-1 cells and promoted the transformation of cell metabolic phenotype from a quiescent to an energetic phenotype (P < 0.05). c LAT2 knockdown significantly decreased glycoPER in MIA PaCa-2 and PANC-1 cells; LAT2 overexpression significantly increased glycoPER in MIA PaCa-2 and PANC-1 cells (P < 0.05). d LAT2 overexpression significantly increased the intracellular level of glutamine in PANC-1 cells. e The expression level of mTOR pathway molecules and key enzymes involved in glycolysis and glutamine metabolism was assessed, and the results revealed that LAT2 upregulated LDHB, PKM2, glutamine synthetase and p-mTOR and downregulated glutaminase. Otherwise, LAT2 did not regulate the expression of LDHA. The data are presented as the mean ± SD. (Student’s t-test; **, P < 0.01)