Figure 6.
Figure 6. 15d-PGJ2 inhibits constitutive NF-κB binding activity and induces apoptosis in different types of B-cell malignancies. (A) Burkitt lymphoma HS-Sultan and BL-41 cells, multiple myeloma U266 and RPMI-8226 cells, and acute leukemia K562 cells (0.5 × 106 cell/mL) were treated with the indicated concentration of 15d-PGJ2 for 3 hours and tested for NF-κB DNA-binding activity by EMSA (left column). The levels of NF-κB DNA-binding activity were quantified by MDP analysis and expressed as arbitrary units (right column). (B) HS-Sultan, BL-41, RPMI-8226, U266, and K562 cells, and healthy donor peripheral blood mononucleated cells (PBMC) were treated with 15d-PGJ2 at the indicated concentrations (control represented by open bars; 5 μM, light gray bars; 10 μM, dark gray bars; 20 μM, filled bars) for 8 hours. Apoptosis was evaluated by FACS analysis of annexin V+ cells.

15d-PGJ2inhibits constitutive NF-κB binding activity and induces apoptosis in different types of B-cell malignancies. (A) Burkitt lymphoma HS-Sultan and BL-41 cells, multiple myeloma U266 and RPMI-8226 cells, and acute leukemia K562 cells (0.5 × 106 cell/mL) were treated with the indicated concentration of 15d-PGJ2 for 3 hours and tested for NF-κB DNA-binding activity by EMSA (left column). The levels of NF-κB DNA-binding activity were quantified by MDP analysis and expressed as arbitrary units (right column). (B) HS-Sultan, BL-41, RPMI-8226, U266, and K562 cells, and healthy donor peripheral blood mononucleated cells (PBMC) were treated with 15d-PGJ2 at the indicated concentrations (control represented by open bars; 5 μM, light gray bars; 10 μM, dark gray bars; 20 μM, filled bars) for 8 hours. Apoptosis was evaluated by FACS analysis of annexin V+ cells.

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