1. A24 induces apoptosis of MCL cells.
A24 induces apoptosis of MCL cells. A and B, MCL chemotherapeutical agents (ara-C and VP-16), but not A24, induce cell cycle arrest. MCL cells were cultured in the presence of VP-16 (100 ng/mL) and ara-C (1 ng/mL), rituximab (10 μg/mL), or A24 (10 μg/mL) for 24 h. Cell cycle was assessed by flow cytometry using propidium iodide after Triton X-100 permeabilization to determine G0-G1, S, and G2-M phases. C, A24 does not alter expression of cell cycle cyclin D1 or p27kip proteins. Protein extracts obtained from UPN1 MCL cell line cultured 72 h in the absence or the presence of A24 were resolved by SDS-PAGE and blotted using anti-cyclin D1 and anti-p27kip antibodies. Antitubulin antibodies were used as a control for sample equal loading. D–F, A24 induces apoptosis of MCL cells. D, UPN1 cells were cultured in the absence or in the presence of 10 μg/mL A24. Apoptosis was evaluated by Annexin V and propidium iodide staining. Numbers indicate the percentage of apoptotic cells. E, MCL cells were cultured in the presence of medium, ara-C (4 ng/mL), or A24 (10 μg/mL). Apoptosis was examined after 24 h by flow cytometry using a mAb against the cleaved form of caspase-3 revealed with an anti-mouse-PE (closed histograms) and compared with corresponding control isotype-PE (open histograms). F, MCL cells were cultured in the presence of medium or A24 (10 μg/mL). Apoptosis was examined by immunoblotting using anti-caspase-9 antibody. Antiactin immunoblotting was used to control for equal protein loading.
Yves Lepelletier et al. Cancer Res 2007;67:
©2007 by American Association for Cancer Research