Fig. 4: CMLD-2, an inhibitor of HuR, has anti-MM effects in vitro.

a Six different MM cell lines were treated with CMLD-2 (0–40 μM) for 48 h, and the viability of these cells was tested by CCK-8 assays. IC₅₀ values from triplicate independent experimental data were calculated from dose‒response curves and are presented as the means ± SDs. b, c CMLD-2 (0 μM, 10 μM, or 20 μM) was added to NCI-H929 and OPM2 cells, after which the cell numbers were recorded for 4 consecutive days after treatment, and the significant differences between the two groups on day 4 were analyzed. d BMMCs isolated from three MM patients (Pt #1, #2, and #3) were treated with CMLD-2 at the indicated concentrations for 48 h, and cell viability was then assessed via CCK-8 assays. e NCI-H929 and OPM2 cells were treated with CMLD-2 (0 μM, 10 μM, or 20 μM) for 48 h, and the early and late apoptosis rates were analyzed. f NCI-H929 and OPM2 cells were treated with CMLD-2 (0 μM, 10 μM, or 20 μM) for 48 h, and the levels of apoptosis-related proteins (PARP1, cleaved PARP1, caspase 3, and cleaved caspase 3) were measured by WB. g, h NCI-H929 and OPM2 cells were treated with CMLD-2 (0 μM, 10 μM, or 20 μM) for 48 h. The cell cycle distribution of NCI-H929 and OPM2 cells was measured by flow cytometry, and the levels of G0/G1 phase-related proteins (CDK4 and cyclin D1) were measured by WB. The data are shown as the means ± SD and were analyzed by one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.