ME1 is required for cell growth and tumorigenicity of human KRAS-mutant CRC cells. (a) Inhibition of ME1 was confirmed by immunoblot. ME1 protein levels were rescued by overexpressing shME1-resistant ME1. β-actin was used as the loading control. (b–d) ME1 suppression inhibits cell growth (b), focus formation (c) and anchorage-independent soft agar growth (d) in KRAS-mutant CRC cells. Restoring ME1 expression rescued the defects in HCT116 and DLD1 cells. Scale bar, 200 μm. Colonies of focus formation and anchorage-independent soft agar were counted and showed in bar graphs. (e) ME1 inhibition attenuated tumor growth (n=5). (f) ME1 activity in xenografts from (e). (g) ME1 inhibition attenuated cell proliferation and increased apoptosis, as indicated by Ki-67 and cleaved caspase-3 staining in xenografts from e. Scale bar, 200 μm. Data are shown as the means±S.D. *P<0.05, **P<0.01, ***P<0.001