Figure 4
Figure 4. Inhibition of the CT-L subunits is sufficient to cause an antitumor effect in MM, NHL, and leukemia tumor cells. (A) PBMC, MM1.S, HS-Sultan, and Molt-4 cells were pulse-treated with 0.18 μM CPSI (c), 0.27 μM IPSI (i), 0.18 μM CPSI plus 0.27 μM IPSI (c + i), 20 nM carfilzomib (CFZ 20 nM), or 10 μM carfilzomib (CFZ 10 μM) for 1 hour, and cell viability was measured at 24 hours. For all datasets, significant differences between the first 2 columns (c or i) and last 3 columns (c + i, CFZ 20 nM, or CFZ 10 μM) were observed (P < .001). (B) MM1.S, HS-Sultan, and Molt-4 cells were 1-hour pulse-treated with compounds as in panel A, and caspase3/caspase 7 activation was monitored at 6 hours for HS-Sultan cells or 9 hours for Molt-4 and MM1.S cells. Representative data from 1 of 4 independent experiments are shown.

Inhibition of the CT-L subunits is sufficient to cause an antitumor effect in MM, NHL, and leukemia tumor cells. (A) PBMC, MM1.S, HS-Sultan, and Molt-4 cells were pulse-treated with 0.18 μM CPSI (c), 0.27 μM IPSI (i), 0.18 μM CPSI plus 0.27 μM IPSI (c + i), 20 nM carfilzomib (CFZ 20 nM), or 10 μM carfilzomib (CFZ 10 μM) for 1 hour, and cell viability was measured at 24 hours. For all datasets, significant differences between the first 2 columns (c or i) and last 3 columns (c + i, CFZ 20 nM, or CFZ 10 μM) were observed (P < .001). (B) MM1.S, HS-Sultan, and Molt-4 cells were 1-hour pulse-treated with compounds as in panel A, and caspase3/caspase 7 activation was monitored at 6 hours for HS-Sultan cells or 9 hours for Molt-4 and MM1.S cells. Representative data from 1 of 4 independent experiments are shown.

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