Fig. 3

Enhanced glycolysis is involved in CCAT1-induced GC malignancy. A, B PCA plot and heatmap showed the DEPs between GC cells with CCAT1 knockdown and control cells. C KEGG pathway analysis indicated that the DEPs mainly enriched in the metabolic pathway. D Volcano plot showed some glycolysis-related proteins were decreased in GC cells with CCAT1 knockdown. E The cBioPortal database suggested that LDHA, PKM2 and HK2 were positively correlated with CCAT1 in GC. F, G qRT-PCR and Western-blot assays showed that the expression of LDHA, HK2, ENO1, GLUT1, PGK1 and PKM2 was significantly reduced and the expression of PKM1 and PKM1/PKM2 were enhanced in GC cells with CCAT1 knockdown, and vice versa. H ECAR was attenuated in GC cells with CCAT1 knockdown and that was elevated in GC cells with CCAT1 overexpression. All data are presented as the mean values ± SD from three independent experiments. Data were evaluated statistically with Multiple unpaired t-tests (G). ^*p < 0.05, ^**p < 0.01