Figure 2
Figure 2. Correlation between BiP/Grp78 levels and MCL sensitivity to bortezomib. (A) BiP/Grp78 protein accumulation after bortezomib treatment was analyzed by Western blot in a panel of 11 MCL cell lines and 7 MCL primary cultures. (B) Relative protein quantification of BiP/Grp78 levels in treated versus control extracts was performed with the use of Image Gauge Fujifilm software and α-tubulin levels for loading normalization. Values were plotted against the respective bortezomib LC50 of each MCL sample (Tables 1 and 2). (C) BiP/Grp78 siRNA and nonsilencing siRNA were transferred to JBR cells by electroporation, and transfected cells were treated with 7.5 or 15nM bortezomib for 15 hours. Viability was assessed by flow cytometry determination of mitochondrial transmembrane potential (ΔΨm) loss, and BiP/Grp78 protein levels were evaluated by Western blot. The results shown are the mean of 2 different experiments (*P < .05).

Correlation between BiP/Grp78 levels and MCL sensitivity to bortezomib. (A) BiP/Grp78 protein accumulation after bortezomib treatment was analyzed by Western blot in a panel of 11 MCL cell lines and 7 MCL primary cultures. (B) Relative protein quantification of BiP/Grp78 levels in treated versus control extracts was performed with the use of Image Gauge Fujifilm software and α-tubulin levels for loading normalization. Values were plotted against the respective bortezomib LC50 of each MCL sample (Tables 1 and 2). (C) BiP/Grp78 siRNA and nonsilencing siRNA were transferred to JBR cells by electroporation, and transfected cells were treated with 7.5 or 15nM bortezomib for 15 hours. Viability was assessed by flow cytometry determination of mitochondrial transmembrane potential (ΔΨm) loss, and BiP/Grp78 protein levels were evaluated by Western blot. The results shown are the mean of 2 different experiments (*P < .05).

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