Fig. 7
From: m6A-dependent glycolysis enhances colorectal cancer progression
The levels of METTL3 and glycolysis components correlate and are clinically relevant in CRC patients. (a) Representative immunohistochemical images of METTL3, HK2 and GLUT1 in CRC tissues using IHC analysis in Cohort 2. Scale bars: 50 μm (400X). Fig. 7a and Figure S7a shared representative immunohistochemical images of METTL3 in METTL3 high expression and METTL3 low expression groups. (b) Correlation between METTL3 expression and HK2 IHC scores in CRC tissues of Cohort 2 (left). Correlation between METTL3 expression and GLUT1 IHC scores in CRC tissues of Cohort 2 (Right), n = 156. (c-e) Smooth estimates of HR (+ 1 UI; increase in recurrence risk for every unit of staining intensity) showed a higher risk of relapse for patients with higher expression of METTL3 (c), HK2 (d) or GLUT1 (e) in Cohort 2. Red dashed lines Indicated 95% confidence interval. (f-h) Kaplan-Meier curves showing the disease-free survival of patients with different levels of METTL3 (f), HK2 (g) or GLUT1 (h) protein intensity in Cohort 2. (i) Smooth estimates of HR (+ 1 UI) showed a higher risk of relapse for patients with higher combined scores of molecular markers (METTL3 + HK2 + GLUT1) in Cohort 2. Red dashed lines Indicated 95% confidence interval. (j) Kaplan-Meier analysis of disease-free survival for CRC patients based on the number of upregulated molecular markers (METTL3, HK2 and GLUT1) in Cohort 2. (k) Inhibition rate of DAA (3-Deazaadenosine) (100 μM) in HCT116 and DLD1 cells. (l-n) Representative images of tumors (l), statistical analysis of tumor volume (m), and weights (n) in nude mice bearing HCT116 and DLD1 cells treated with DAA. (o) Schematic diagram of the relationship among METTL3, m6A modification, colorectal cancer cell progression and glycolysis metabolism