Fig. 2
The high MYC expression contributes to the RR phenotype. a The SRR2 luciferase activity in RR cells derived from SupM2 and Karpas 299 cells with scr siRNA or MYC siRNA transfection. The western blots below showed the knockdown efficiency of MYC. b The SRR2 luciferase activity in RR cells with the treatment of 10 μM 10074-G5 for 24 h. Cells with DMSO treatment were used as a negative control. c RU and RR cells derived from both cell lines were transiently transfected with pcDNA3.3-MYC (i.e., MYC). pcDNA empty vector (EV) was included as a negative control. The western blots showed the MYC transfection efficiency. Below shows the SRR2 luciferase activity in RU and RR cells with either EV or MYC transient transfection. d The clonogenicity of RR cells in the presence of 5 μM 10074-G5 by using the methylcellulose colony formation assay. Cells with DMSO treatment were included as a control. The relative colony numbers analyzed in triplicate were shown in the lower panel. The colony will be counted if only its size is equal or larger than the one that was pointed by the bolded arrow. One representative result was shown here. e The cell growth inhibition in RR cells originated from SupM2 and Karpas 299 induced by the treatment of doxorubicin (20 and 50 ng/mL, respectively), or 10074-G5 (5 μM), or combination of the doxorubicin and 10074-G5 for 48 h, assessed by the MTS assay. f The cell growth inhibition induced by varying doses of doxorubicin for 48 h in RU cells derived from SupM2 with either EV or MYC transient transfection, assessed by the MTS assay. g The clonogenicity of RU and RR cells from SupM2 with either EV or MYC transient transfection, assessed by the methylcellulose colony formation assay. The relative colony numbers analyzed in triplicate were shown in the lower panel. The colony will be counted if only its size is equal or larger than the one that was pointed by the bolded arrow. One representative result was shown here