Fig. 7
Expression of free NHR2 domain of CBFA2T3 delays BCP-ALL cell proliferation. a and b Proliferation curves from REHshcontrol, REHshRUNX1, REHshCBFA2T3−1, REHshCBFA2T3−2 (a), or REHshcontrol and REH+NHR2 cells (b). Three experiments are represented for each condition. For more readability, statistical analyses have been run only for the last day (day 7) and compared to the condition REHshcontrol. * p < 0.05. c, d Kaplan–Meier survival curves from immunodeficient NOD/scid IL2 Rg null mice xenografted with 100,000 cells of REH, REHshRUNX1, REHshCBFA2T3−1, REHshCBFA2T3−2 (C), or REH+NHR2 (D) (n = 7–8 per group). The general condition of mice was monitored daily until experiment ended. Mantel-Cox statistical tests compared to the condition REHshcontrol. **p < 0.01, ***p < 0.001. e We propose the model in which CBFA2T3 acts as an activator of RUNX1 transcription activity and sustains cell proliferation. Presence of free NHR2 domain disrupts this activation complex and slows down proliferation