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. 2020 Jan 29;14(4):763–778. doi: 10.1002/1878-0261.12641

Figure 1.

Figure 1

Inhibition of autophagy sensitizes NEK2‐OE MM cells to BTZ. (A) Representative images of immunofluorescence analysis for NEK2 (green) and LC3B (red) protein expression in CD138+ cells derived from HD (n = 6), NDMM patients (n = 9), and RMM patients (n = 7). (B) KMS11 EV, KMS11 NEK2‐OE, RPMI 8226 EV, and RPMI 8226 NEK2‐OE MM cells were treated with different doses of CQ (0, 10 μm, 20 μm, 40 μm) in combination or not with BTZ (10 nm), and cell viability was examined 48 h later. (C) Clonogenic analysis of KMS11 EV, KMS11 NEK2‐OE, RPMI 8226 EV, and RPMI 8226 NEK2‐OE MM cells after treatment with CQ (0, 10 μm, 20 μm) in combination or not with BTZ (1 nm), respectively (4×). (D) Western blots of full‐length PARP, cleaved PARP, cleaved caspase‐3, NEK2, and β‐actin in KMS11 EV, KMS11 NEK2‐OE, RPMI 8226 EV, and RPMI 8226 NEK2‐OE MM cells after treatment with CQ (0, 10 μm, 20 μm) in combination with or not with BTZ (10 nm). The ratio of integrated density between cleaved PARP and full‐length PARP was shown under the band of PARP. Scale bar: 5 μm. ns P > 0.05, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Significance was determined by Student’s t‐test. Error bars indicate SD.