American Society of Hematology

Figure 7.

$Figure 7. CDDO-Im + bortezomib triggers apoptosis in bortezomib-resistant cancer cells. (A) CDDO-Im and bortezomib decrease survival in Bcl2-overexpressing MM.1S cells. MM.1S cells were stably transfected with Bcl2 construct; treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours; and assessed for viability using MTT assays. Results are mean ± SD of 4 independent experiments (P < .004). (B) CDDO-Im and bortezomib induce apoptosis in SUDHL4 (DHL4) lymphoma cells expressing high levels of heat shock protein-27 (Hsp27). DHL4 cells were treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours and assessed for apoptosis by DNA fragmentation assays. Results are mean ± SD of 4 independent experiments (P < .005). (C) CDDO-Im and bortezomib induce apoptosis in RC-K8 lymphoma cells with genetically inactivated IκB-α protein and high intrinsic activation of NF-κB. RC-K8 cells were treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours and assessed for apoptosis by DNA fragmentation assays. Results are mean ± SD of 4 independent experiments (P < .005). (D) CDDO-Im + bortezomib induces apoptosis in bortezomib-resistant patient MM cells. CD138+ cells were freshly isolated from an MM patient (patient no. 1) refractory to bortezomib; treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours; and cytosolic proteins separated by 12.5% SDS-PAGE and analyzed for apoptosis by immunoblotting with anti-PARP Abs (top panel). Blots are representative of 3 independent experiments. FL indicates full length, and CF denotes cleaved fragment. Apoptosis was also assessed by annexin V staining in CDDO-Im + bortezomib-treated MM cells from patient no. 1 (middle panel) and patient no. 2 (bottom panel). Percent positive annexin V cells shown are mean ± SD of triplicate samples.$

CDDO-Im + bortezomib triggers apoptosis in bortezomib-resistant cancer cells. (A) CDDO-Im and bortezomib decrease survival in Bcl2-overexpressing MM.1S cells. MM.1S cells were stably transfected with Bcl2 construct; treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours; and assessed for viability using MTT assays. Results are mean ± SD of 4 independent experiments (P < .004). (B) CDDO-Im and bortezomib induce apoptosis in SUDHL4 (DHL4) lymphoma cells expressing high levels of heat shock protein-27 (Hsp27). DHL4 cells were treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours and assessed for apoptosis by DNA fragmentation assays. Results are mean ± SD of 4 independent experiments (P < .005). (C) CDDO-Im and bortezomib induce apoptosis in RC-K8 lymphoma cells with genetically inactivated IκB-α protein and high intrinsic activation of NF-κB. RC-K8 cells were treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours and assessed for apoptosis by DNA fragmentation assays. Results are mean ± SD of 4 independent experiments (P < .005). (D) CDDO-Im + bortezomib induces apoptosis in bortezomib-resistant patient MM cells. CD138⁺ cells were freshly isolated from an MM patient (patient no. 1) refractory to bortezomib; treated with CDDO-Im, bortezomib, or CDDO-Im + bortezomib for 24 hours; and cytosolic proteins separated by 12.5% SDS-PAGE and analyzed for apoptosis by immunoblotting with anti-PARP Abs (top panel). Blots are representative of 3 independent experiments. FL indicates full length, and CF denotes cleaved fragment. Apoptosis was also assessed by annexin V staining in CDDO-Im + bortezomib-treated MM cells from patient no. 1 (middle panel) and patient no. 2 (bottom panel). Percent positive annexin V cells shown are mean ± SD of triplicate samples.

This Feature Is Available To Subscribers Only