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. 2019 Apr 24;105(1):136–147. doi: 10.3324/haematol.2018.212365

Figure 2.

Figure 2.

Inhibition of E-selectin leads to an increase of Scl/Tal1 in BCR-ABL1+ leukemia-initiating cells. (A) Schematic of an in vitro adhesion assay, in which 20,000 GFP+ (BCR-ABL1+) Lin− c-Kit+ bone marrow cells from mice with chronic myeloid leukemia treated with vehicle, GMI-1271, imatinib or the combination of GMI-1271 plus imatinib were plated on recombinant E-selectin in the presence of the respective drugs for 6 h. (B) Percentage of adherent GFP+ (BCR-ABL1+) Lin− c-Kit+ of total cells after 6 h of incubation on recombinant E-selectin in the presence of vehicle (black), 20 mM GMI-1271 (dark gray), 10 mM imatinib (light gray) or imatinib plus GMI-1271 (white) and several washing steps, normalized by the number of live cells. Twenty thousand cells per well were plated in triplicate. The percentage of adherent cells was reduced by treatment with GMI-1271 or imatinib plus GMI-1271 compared to vehicle [P=0.02 or P=0.029, respectively, analysis of variance (ANOVA); Tukey test, n=4]. (C) Relative expression of Scl/Tal1 in all GFP+ (BCR-ABL1+) Lin− c-Kit+ cells plated on recombinant E-selectin as in (A) and (B) in the presence of vehicle (black), GMI-1271 (dark gray), imatinib (light gray) or imatinib plus GMI-1271 (white). The expression of Scl/Tal1 in GMI-1271-treated cells was significantly increased compared to that of vehicle-treated cells (P=0.017, ANOVA; Tukey test, n=3). BM: bone marrow; CML: chronic myeloid leukemia; qPCR: real-time polymerase chain reaction.