MOESM9 of LncRNA LINRIS stabilizes IGF2BP2 and promotes the aerobic glycolysis in colorectal cancer

Additional file 9: Figure S4, related to Fig. 4. The alteration of MYC-mediated glycolysis under the influence of LINRIS. (A) The mRNA levels of MYC and downstream genes, including GLUT-1, PKM2 and LDHA, when inhibiting LINRIS in DLD-1 cells. The data are shown as the mean ± SD; n = 3 independent experiments, two-tailed Student’s t-test, *P < 0.05, **P < 0.01. (B) BrdU assay showing that the overexpression (OE) of IGF2BP2 partially rescued the proliferation inhibition of DLD-1 cells with the knockdown of LINRIS. The data are shown as the mean ± SD; n = 3 independent experiments, two-tailed Student’s t-test, *P < 0.05, **P < 0.01. (C) The ECAR was detected in DLD-1 cells with or without sh-1 and overexpressed IGF2BP2 using an XF Extracellular Flux Analyzer. Glucose, oligomycin and 2-DG were injected sequentially at different time points as indicated. The data shown represent three independent experiments. (D) Overexpression of IGF2BP2 partially reversed the suppression of LINRIS knockdown on glycolytic activity in DLD-1 cells. The data are shown as the mean ± SD; n = 3 independent experiments, two-tailed Student’s t-test, *P < 0.05, **P < 0.01. (E) BrdU assay showing that the overexpression (OE) of the K139 mutant of IGF2BP2 completely rescued the proliferation inhibition of the indicated cells with knockdown of LINRIS. The data are shown as the mean ± SD; n = 3 independent experiments, two-tailed Student’s t-test, *P < 0.05, **P < 0.01.