Fig. 6From: RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion, and inhibition of the ubiquitin–proteasome pathway contributes to the reversion of ATRA resistanceMG132 combined with ATRA induced GTF2I-RARA-positive cell differentiation. GTF2I-RARA-positive HL60 cells were treated with various concentrations of MG132 and 1 μM of ATRA for 3 days. a The myeloid differentiation marker CD11b was assessed by flow cytometry. The percentage of CD11b-positive cells increased in a dose-dependent manner on the cells treated with MG132 in combination with ATRA. Results are represented in the form of mean values ± standard deviations from three independent experiments. *p < 0.05, **p < 0.01. b When GTF2I-RARA-positive cells were exposed to ATRA (1.0 μM) and MG132 (0.2 μM), they manifested distinctly different characteristics (×1000)Back to article page