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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: miR-3189-targeted GLUT3 repression by HDAC2 knockdown inhibits glioblastoma tumorigenesis through regulating glucose metabolism and proliferation

Fig. 5

miR-3189 regulates glucose metabolism through GLUT3 inhibition in HDAC2 knockdown GBM cells. A Glucose uptake in DOX-inducible shHDAC2 GBM cells. B Metabolism schematic diagram of HDAC2 knockdown GBM cells. C Cell death analysis in GLUT3 siRNA-transfected DOX-inducible shHDAC2 GBM cells w/wo doxycycline by using western blot with indicated antibodies. D Cell death analysis in miR-3189 mimic-transfected DOX-inducible shHDAC2 GBM cells w/wo doxycycline by using western blot with indicated antibodies. E-F Glucose uptake in DOX-inducible shHDAC2 GBM cells using GLUT3 siRNA (E) or miR-3189 mimics (F). G-H Lactate production in DOX-inducible shHDAC2 GBM cells using transfected with either GLUT3 siRNA (G) or miR-3189 mimics (H). I-J Cell proliferation of DOX-inducible shHDAC2 GBM cells using GLUT3 siRNA (I) or miR-3189 mimics (J). K-L Mitochondrial versus non-mitochondrial metabolism in DOX-inducible shHDAC2 GBM cells w/wo doxycycline. Time-dependent Oxygen Consumption Rate (OCR, K) measurements and Extracellular Acidification Rate (ECAR, L) measurements were traced with a Seahorse Bioscience XF96 analyzer. Data are expressed as the mean ± SD for triplicates. One-way ANOVA with multiple comparisons correction (p < 0.001). All data are expressed as the mean ± SD from three independent experiments, each performed in triplicate. **p < 0.01, ***p < 0.001

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