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. 2017 Dec 30;12(2):180–195. doi: 10.1002/1878-0261.12157

Figure 4.

Figure 4

(A) The expression of CRBN at mRNA level was not restored after treatment of the resistant cells with 5‐Aza, EPZ‐6438, or their combination, suggesting that the downregulation of CRBN, which is observed in all the IMiD‐resistant cells with acquired resistance, might not have a direct causality to the development of resistance. (B) Western blot of IKZF1 in OPM2, OPM2‐PR, and OPM2‐PR cells after treatment with 5‐Aza and EPZ‐6438. All the cells were either untreated or treated with lenalidomide or pomalidomide (10 μm) for 24 h, at which point cell lysates were isolated. The CRBN‐dependent degradation of IKZF1 after treatment with IMiDs is reduced in OPM2‐PR, but is partly rescued in the resensitized OPM2‐PR cells. (C) Apoptosis response in primary IMiD‐resistant cell lines JJN3, LP1, and RPMI‐8226, showing that the combination of 5‐Aza and EPZ‐6438 – or EZH2 inhibition alone (in the case of JJN3), can also overcome intrinsic resistance to IMiDs. **P < 0.01, ***P < 0.001, and ****P < 0.0001.