Alternative pathways of programmed cell death are activated in cells with defective caspase-dependent apoptosis
| Authors | |
|---|---|
| Year of publication | 2008 |
| Type | Article in Periodical |
| Magazine / Source | Leukemia Research |
| MU Faculty or unit | |
| Citation | |
| Field | Oncology and hematology |
| Keywords | apoptosis; autophagy; programmed cell death |
| Description | Loss of programmed cell death pathways is one of the features of malignancy that complicate the response of cancer cells to therapy. Activation of alternative death pathways offers a promising approach to enhance efficiency of cancer chemotherapy. We analysed programmed cell death pathways of v-myb-transformed BM2 monobolasts induced by arsenic trioxide, cycloheximide and camptothecin. We show that cell death is not executed by caspases but rather by alternative cell death pathways: camptothecin induces the lysosome-dependent cell death, arsenic trioxide induces autophagy, and most of cycloheximide-treated BM2 cells die by necrosis. The fact that alternative cell death pathways can be switched in cells with defects in activation and/or function of caspases suggests that understanding and targeting of these pathways could improve therapy on cancer cells suffering from defective apoptosis. |
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