Figure 6. NDRG2 inhibits the growth and proliferation of colorectal cancer cells.
A. Equal numbers of NDRG2-overexpressing HCT116 (HT-29) cells and control cells were seeded onto 60 mm dish. After 14 days, the cells were fixed and stained with crystal violet. B. Mice were injected subcutaneously in the right limb with 1 × 107 NDRG2-overexpressing or control HCT116 (HT-29) cells respectively. Representative tumor formation was photographed 28 days after injection. C. Tumors volume was calculated by the formula (width2 × length × 0.5). D. Tumor weight of mice was calculated 28 days after injection. All *P < 0.05; **P < 0.01. E. A suggested model for the regulation of metabolic pathways in colorectal cancer cells by tumor suppressor NDRG2. NDRG2 inhibited glycolysis via regulating glucose transporter GLUT1, glycolytic enzymes HK2, PKM2 and LDHA. NDRG2 also inhibited glutaminolysis via regulating glutamine transporter ASCT2 and glutaminase GLS1 in colorectal cancer cells. Transcriptional factor c-Myc mediated inhibition of glycolysis and glutaminolysis by NDRG2. Moreover, NDRG2 inhibited intracellular β-catenin levels and TCF/LEF transcription activity, which lead to the transcriptional inhibition of C-MYC gene.