Skip to main content
Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: LAT2 regulates glutamine-dependent mTOR activation to promote glycolysis and chemoresistance in pancreatic cancer

Fig. 2

LAT2 decreases gemcitabine sensitivity in vitro and in vivo. a, c LAT2 knockdown by siLAT2 significantly increased gemcitabine sensitivity in MIA PaCa-2 and PANC-1 cells. b, d LAT2 overexpression by LAT2 OE plasmids significantly decreased gemcitabine sensitivity in MIA PaCa-2 and PANC-1 cells. e, g LAT2 knockdown decreased the extracellular acidification rate (ECAR) in MIA PaCa-2 and PANC-1 cells and resulted in an evident reduction in ECAR in MIA PaCa-2 and PANC-1 cells exposed to gemcitabine (10 μM) for 24 h. f, h LAT2 overexpression increased ECAR in MIA PaCa-2 and PANC-1 cells and resulted in an evident reduction in ECAR in MIA PaCa-2 and PANC-1 cells exposed to gemcitabine (10 μM) for 24 h. i In nude mice treated with gemcitabine or PBS, the tumors generated from pLVX-PANC-1-LAT2 cells grew significantly faster than those generated from the control cells; The tumors generated from cells with a high LAT2 level were significantly larger than those generated from control cells two weeks after treatment with gemcitabine or PBS; The tumor growth inhibition (TGI) rate of the tumors generated from pLVX-PANC-1-LAT2 cells was significantly lower than that of the tumors generated from the control cells. j The tumor weight in the pLVX-PANC-1-LAT2 group was significantly heavier than that in the control group. k In LAT2 control group, the tumor volume in the GEM treatment group was significantly smaller than that in the PBS control group; In LAT2 OE group, the tumor volume in the GEM treatment group was similar with that in the PBS control group. The data are presented as the mean ± SD. (Student’s t-test; *, P < 0.05)

Back to article page