Apoptosis is one of the major mechanisms of
photodynamic therapy (
PDT) that leads to
tumor degradation. Apoptosis-related genes and
proteins function in a certain order and timing in the complex network of apoptosis. To further understanding of the apoptotic mechanism of
PDT, this research examined the time course of apoptosis from PsD007 (a second-generation
photosensitizer developed in China) induced
PDT on the rat
acute myeloid leukemia cell line LT12. MTT was used to detect the temporal dynamic of
PDT killing effects and identified the "apoptotic window" of 2-24 h. Apoptosis showed a basal peak at 2 h, and the duration of apoptosis depended on
PDT dose, which disappeared quickly at low concentrations but lasted to higher levels to 6 or 12 h at high concentrations as detected by flow cytometry. High-content imaging confirmed these results. An 84-gene apoptosis PCR array identified 15 genes with an expression level change of over twofold at 6 h post-
PDT. Nine apoptosis-related genes showed changes in expression at 2-12 h after
PDT. TNF family genes TNF and FASLG showed a maximal change of 3.47- and 4.42-fold from baseline. Key apoptosis
proteins such as activated
caspases showed strong up-regulation after
PDT, with the expression peaks of cleaved
caspase-7,
caspase-9 and PARP at 4-6 h, and cleaved
caspase-3 delayed to 6-12 h. Our findings help clarify the time course of apoptosis events in response to
PDT treatment in a
leukemia cell line and may help contribute to the clinical application of
PDT in
leukemia treatment.