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Fig. 1 | Cancer Cell International

Fig. 1

From: 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 resistance

Fig. 1

Effects of GTF2I-RARA blocking ATRA-induced differentiation and conferring proliferation potential in the HL60 cell line. a Western blot confirmed the stable expression of GTF2I-RARA in HL60. b NB4 cells or GTF2I-RARA-HL60 cells were treated with different doses of ATRA. PML-RARA or GTF2I-RARA was visualized by western blot 48 h after ATRA treatment. β-actin was used as the loading control. c MTT assay results for evaluating the proliferation potential in GTF2I-RARA-positive HL60 cells. Cells were exposed to different dosages of ATRA for 24 h, 48 h, and 72 h, and the proliferation-inhibiting rate is shown. The results were in the form of mean values ± standard deviations corresponding to at least three independent experiments. Statistical significance was determined with Student’s t test. *p < 0.05, **p < 0.01. d Flow cytometry analysis of cell surface CD11b in GFP-positive HL60 cells and NB4 cells at 24 h, 48 h, and 72 h after incubation in different dosages of ATRA or ethanol solvent. e Evaluation of morphology for cell differentiation in GTF2I-RARA-positive HL60 cells or NB4 cells 72 h after treatment with 1 μM of ATRA and staining with hematoxylin and eosin

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