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. Author manuscript; available in PMC: 2022 Aug 1.
Published in final edited form as: Mol Cancer Ther. 2021 Dec 14;21(2):347–358. doi: 10.1158/1535-7163.MCT-21-0310

Figure 5. Treatment with 5-Fu overcomes MM resistance to BTZ induced by OB-Runx2 deficiency.

Figure 5.

A, Schematic diagram of the tumor injection and treatment schedule for mice used in experiments in B-E. 5-week-old OB-Runx2−/− and OB-Runx2+/+ mice were i.v. injected with 5TGM1-Luc MM cells (down arrow) 1 week before treatment with PBS, BTZ, 5-Fu, or BTZ+5-Fu (left up arrow) for 4 weeks. Blood and BM were collected at study end (right up arrow) for all analyses (n=5–7 mice/group). B, Representative bioluminescence imaging of OB-Runx2−/− and OB-Runx2+/+ mice after treatment (left); graphical representation of the luminescence intensity in each group (right) (n=5–7 mice/group). C, Quantification of serum IgG2bκ concentration in mice after treatment, measured by ELISA in duplicate (n=5–7 mice/group). D, Flow cytometry gating strategy for identifying CD138+, Ki-67+, and cleaved caspase-3-positive cells among BM cells harvested after treatment (n=5 mice/group). E-G, Percentage of CD138+ MM cells detected among all B220+ B cells (E) and the percentage of Ki-67+ MM cells (F) and cleaved caspase-3+ MM cells (G) detected among the CD138+ cells. Data are presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.001. ns, not significant.