Thapsigargin induces a calmodulin/calcineurin‐dependent apoptotic cascade responsible for the death of prostatic cancer cells

New agents are required for the treatment of androgen‐independent prostate cancer. Due to the low rate of proliferation of these malignant cells, agents which can activate the apoptotic death of these cells without requiring the cells being in the proliferative cell cycle are critically required. Thapsigargin (TG), via its ability to perturb intracellular free calcium [Ca2+]i, is such a cell proliferation‐independent cytotoxic agent. The present study focuses on more completely describing the biochemical cascade during the apoptotic death of androgen‐independent prostate cancer cells induced by TG and on the mechanistic requirements for this death.

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