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The mechanism of TAM-induced apoptosis in human BDC is unclear. To understand more about it, we examined the expression of p53 protein, which is associated with apoptosis after TAM treatment. P53 is a tumor suppressor gene product. Induction of apoptosis is an essential function of p53. It activates downstream genes in a sequence-specific manner to induce apoptosis [13]. In our study, when Perifosine were treated with TAM, the level of p53 increased significantly. This result implies that p53 might play an important role in TAM-induced apoptosis in QBC939 cells.
There are several signaling pathways that lead to the activation of apoptotic machinery [14]. During the past few years, rapid advances in the molecular understanding of apoptotic mechanism have identified numerous pathways for cell death. The execution phase involves a series of morphologic and biochemical changes that appear to result from the action of cysteine-dependent aspartate-directed proteases called caspases. Of these cysteine proteases, caspase-3 is believed to be one of the most commonly involved in the implementation of apoptosis in various cell types [15]. In chemiosmosis study, we measured the activity of caspase-3; the results demonstrated that caspase-3 activity was increased significantly in a TAM dose- and time-dependent manner in QBC939 cells.