Fig. 2: SNHG14 was upregulated in glioma and knockdown of SNHG14 suppressed glycolysis and proliferation. | Cell Death & Disease

Fig. 2: SNHG14 was upregulated in glioma and knockdown of SNHG14 suppressed glycolysis and proliferation.

From: Lin28A promotes IRF6-regulated aerobic glycolysis in glioma cells by stabilizing SNHG14

Fig. 2

a The expression of SNHG14 in glioma tissues and NBTs. Data are presented as the mean ± SD (n = 8 in each group). *P < 0.05, **P < 0.01 versus NBTs group. b The expression of SNHG14 in NHA, U87 and U251. Data are presented as the mean ± SD (n = 3 in each group). *P < 0.05, **P < 0.01 versus NHA group. c ECAR was measured to detect the effect of SNHG14 depletion and re-expression on glycolysis. d, e The lactate production and glucose uptake in response to SNHG14 depletion and re-expression. f Expression of PKM2 and GLUT1 by western blot upon SNHG14 depletion and re-expression. g CCK-8 assay was conducted to investigate the effect of SNHG14 in cell proliferation. h Flow cytometry analysis was used to evaluate the function of SNHG14 in apoptosis. Data are presented as the mean ± SD (n = 3, each group). **P < 0.01 versus sh-SNHG14-NC group, ##P < 0.01 versus sh-SNHG14 + SNHG14-NC group. One-way analysis of variance was used for statistical analysis.

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