Fig. 4

Effect of knockdown of LHX9 on the reprogramming of glycolytic metabolism and malignant biological properties of GCSCs. A: RT-qPCR and Western Blot to detect the effect of knockdown of LHX9 on PKM2 activity in GCSCs; B: changes in lactate levels in GCSCs after knockdown of LHX9; C: changes in ATP expression in GCSCs after knockdown of LHX9; D: RT-qPCR and Western Blot to detect the effect of knockdown of LHX9 on GCSCs transcriptional activity and protein expression changes of glycolysis-related genes (GLUT1, HK2, LDHA, and PDK1) in GCSCs after knockdown of LHX9; E–F: CCK-8 and EDU assays to detect the effect of knockdown of LHX9 on the proliferation ability of GCSCs; G-H: Transwell and scratch assays to detect the effect of knockdown of LHX9 on the migration and invasion ability of GCSCs; NC: Human normal gastric epithelial cells (GSE-1); sh-NC: GCSCs transfected with sh-NC by lentivirus; sh-LHX9: GCSCs transfected with knockdown LHX9 by lentivirus; *: P < 0.05, statistically significant comparison between groups; Data comparison between the two groups was conducted using an independent samples t-test. For different time points, a two-factor analysis of variance (ANOVA) was employed to analyze the cellular data. The cell experiments were repeated three times