FIGURE 2.

Direct manipulation of c‐Myc has no effects on thiopurine drug resistance. A, Western blot analysis of oncogene c‐Myc in Namalwa after treating with increasing concentrations of c‐Myc inhibitor 10058‐f4 (0, 10, 20, 30 µg/mL) for 48 h. β‐Actin was used as a loading control. B, Apoptosis of Namalwa after treating for 48 h with increasing concentrations of c‐Myc inhibitor 10058‐f4 (0, 10, 20, 30 µg/mL). *: P < 0.05; two‐tailed Student's t tests. C, The 6‐mpIC50 of Burkitt's lymphoma cells including Namalwa, Daudi and Raji treated with or without 20 µg/mL c‐Myc inhibitor 10058‐f4 for 48 h. P > 0.05; two‐tailed Student's t tests. D, Heatmap showing metabolomics analysis of Namalwa after treating with or without 20 µg/mL c‐Myc inhibitor 10058‐f4. E, c‐Myc and PRPS1/2 in a Western blot analysis of sh‐c‐Myc Raji cells. β‐Actin was used as a loading control. f, Cell viability of sh‐c‐Myc Raji cells at increasing concentrations of 6‐mp. P > 0.05; two‐tailed Student's t tests. G, Heatmap showing intracellular steady‐state metabolite profiles of sh‐c‐Myc Raji cells. H, Western blot of c‐Myc and PRPS1/2 in c‐Myc overexpressed Vocb6cells. β‐Actin was used as a loading control. I, The IC50 of thiopurines in c‐Myc overexpressed Vocb6cells. P > 0.05; two‐tailed Student's t tests. J, Heatmap showing intracellular steady‐state metabolite profiles of cell lines in (H). K, Western blot of c‐Myc and PRPS1/2 in sh‐c‐MycVocb6cells. β‐Actin was used as a loading control. L, Testing the 6‐mpIC50 of Vocb6sh‐c‐Myc cell line. P > 0.05; two‐tailed Student's t tests. M, Heatmap showing purine metabolite profiles of cell lines in (K)