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. 2021 Apr 2;218(5):e20191360. doi: 10.1084/jem.20191360

Figure 5.

Figure 5.

A soft ECM increases NF-κB signaling to regulate JNK activity and apoptosis. (A) Western blot showing bands for phosphorylated c-Jun (Ser63) in MCF10A cells stably transduced with a dominant-negative IκBαM mutant or the vector backbone and cultured on soft or stiff substrates at indicated time points after 10 nM paclitaxel treatment. (B) Bar graph showing mean ± SEM with individual values of Western blot quantifications of phosphorylated c-Jun (Ser63) by pixel density normalized to E-cadherin loading control in MCF10A cells stably transduced with a dominant-negative IκBαM mutant or the vector backbone and cultured on soft or stiff substrates at indicated time points after 10 nM paclitaxel treatment (n = 4). (C) Bar graph showing mean ± SEM with individual values of the percentage of cleaved caspase 3–positive cells from MCF10A cells expressing a dominant-negative IκBαM mutant cultured on soft or stiff substrates and treated with 10 nM paclitaxel or vehicle. (D) Bar graph showing mean ± SEM with individual values of the percentage of cleaved caspase 3–positive cells from HCC70 cells expressing a dominant-negative IκBαM mutant cultured on soft or stiff substrates and treated with 100 nM paclitaxel, 100 nM paclitaxel with 5 µM SP600125, or vehicle. Unless otherwise noted, n = 3 for all experiments. All statistical analyses were performed using two-tailed t test (*, P < 0.05; **, P < 0.01).