FIGURE 1.

MSI2 expression was elevated in glioma tissues and cells, and knockdown of MSI2 suppressed glycolipid metabolism and proliferation. (A) Expression of MSI2 is high in glioma from TCGA database. (B) Expression of MSI2 in NBTs and glioma from TCGA samples. (C) Effect of MSI2 expression level on LGG patient survival time from TCGA database. (D) Protein level of MSI2 was analyzed in normal brain tissues (NBTs), low‐grade gliomas (LGGs), and high‐grade gliomas (HGGs) via Western blot. ^* p < .05 versus NBTs group; ^** p < .01 versus NBTs group; ^## p < .01 versus LGGs group. (E) MSI2 protein level was analyzed in normal human astrocytes (NHA) and glioma cell lines (U251 and U373) via Western blot. ^** p < .01 versus NHA group. (F) HK2 and ACLY protein expression after MSI2 knockdown in U251 and U373 cells was analyzed via Western blot. (G and H) The effect of MSI2 knockdown on glycolysis in U251 and U373 cells was analyzed via extracellular acidification rate (ECAR), including glycolysis and glycolytic capacity. (I and J) Lactate production and glucose uptake were measured in U251 and U373 cells after MSI2 knockdown. (K and L) Intracellular triglyceride and cholesterol expression levels were measured after MSI2 knockdown. ^* p < .05 versus MSI2(−)NC group; ^** p < .01 versus MSI2(−)NC group. (M) Representative confocal fluorescence imaging of lipid droplets (LDs) stained by BODIPY 493/503 (green) in U251 and U373 cells. Nucleus (blue) was stained by DAPI. Scale bars = 20 μm. Data are presented as the mean ± SD (n = 15, each group). ^** p < .01 versus MSI2(−)NC group. (N) Effect of MSI2 on the proliferation of U251 and U373 cells was detected via Cell Counting Kit‐8 (CCK‐8) assay. ^** p < .01 versus MSI2(−)NC group. Except for specially noted, data are presented as the mean ± SD of three independent experiments per group. One‐way ANOVA was used for statistical analysis