Figure 3
Figure 3. Bortezomib transiently repressed the expression of HR genes at the transcriptional level. (A) MM cell lines were treated with 2.5nM bortezomib and harvested at the indicated times. FANCD2, RAD-51, BRCA1, and BRCA2 mRNA levels were determined by qRT-PCR. Data quantification was carried out by the 2−ΔΔCt method. (B-C) MM1S cells transfected with a pSGG_prom vector (SwitchGear genomics) that contains an approximately 3-kb fragment of the human promoter for BRAC1, BRAC2, FANCD2, RAD51, or GAPDH (control) cloned into the MCS and fused to a luciferase reporter gene. Transfected cells were treated with a nonlethal dose(s) of bortezomib alone (B), the NF-κB inhibitor SN50 (C), or vehicle control (CNT) for 24 hours and then assayed for their luciferase activity. Signal was read out on a luminometer.

Bortezomib transiently repressed the expression of HR genes at the transcriptional level. (A) MM cell lines were treated with 2.5nM bortezomib and harvested at the indicated times. FANCD2, RAD-51, BRCA1, and BRCA2 mRNA levels were determined by qRT-PCR. Data quantification was carried out by the 2−ΔΔCt method. (B-C) MM1S cells transfected with a pSGG_prom vector (SwitchGear genomics) that contains an approximately 3-kb fragment of the human promoter for BRAC1, BRAC2, FANCD2, RAD51, or GAPDH (control) cloned into the MCS and fused to a luciferase reporter gene. Transfected cells were treated with a nonlethal dose(s) of bortezomib alone (B), the NF-κB inhibitor SN50 (C), or vehicle control (CNT) for 24 hours and then assayed for their luciferase activity. Signal was read out on a luminometer.

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