Fig 1: OTX015 suppresses the drug resistance induced by BRD2 in T‐LBL cells. A. The cell viability was measured by MTT assay in control cells (Jurkat and SUP‐T1), Dox‐treated cells (Jurkat+Dox and SUP‐T1+Dox), BRD2‐overexpressing cells treated with Dox (Jurkat‐BRD2+Dox and SUP‐T1‐BRD2+Dox), and BRD2‐overexpressing cells treated with Dox and OTX015 (Jurkat‐BRD2+Dox+OTX015 and SUP‐T1‐BRD2+Dox+OTX015). Results are presented as mean ± SD of three independent experiments; *, comparison between control group and BRD2‐overexpressing group, P < 0.05; #, comparison between BRD2‐overexpressing group and BRD2‐overexpressing + OTX015 group, P < 0.05. B. Dox‐induced apoptosis was detected by Annexin V/PI staining and flow cytometry assays in control BRD2‐overexpressing Jurkat and SUP‐T1 cells (Control), BRD2‐overexpressing Jurkat and SUP‐T1 cells treated with Dox (+Dox), and BRD2‐overexpressing Jurkat and SUP‐T1 cells treated with Dox and OTX015 (+Dox+OTX015). C. The protein expression levels of p‐ERK, ERK, p‐MEK, MEK, RasGRP1, and c‐Myc were detected by Western blotting in BRD2‐overexpressing Jurkat and SUP‐T1 cells treated with Dox alone or both Dox and OTX015. The protein expression of β‐actin was used as loading control. D. The relative mRNA levels of RasGRP1 were measured by semi‐quantitative real‐time PCR assay in BRD2‐overexpressing Jurkat and SUP‐T1 cells treated with Dox alone or both Dox and OTX015. Results are presented as mean ± SD of three independent experiments; *, P < 0.05. Abbreviations: T‐LBL, T‐cell lymphoblastic lymphoma; Dox, doxorubicin; SD, standard deviation