The present study aimed to investigate the effect, and elucidate the potential mechanisms, of 9-hydroxypheophorbide α-based
photodynamic therapy (9-HPbD-PDT) on apoptosis and
necrosis induction, and migration suppression of
laryngeal cancer AMC-HN-3 (HN-3) cells.
Phototoxicity initiated by 9-HPbD-PDT on
HN-3 cells was observed in a
photosensitizer dose-dependent pattern. There was an initial increase of apoptotic cells coupled with gradual enhancement of reactive
oxygen series (ROS) generation at lower doses of 9-HPbD. By contrast, at a higher dose of 9-HPbD, there was a clear increase of necrotic cells with a gradual decrease of ROS generation. Following
PDT, an elevated percentage of apoptotic cells with shrinkage or condensing nuclei was observed using
Hoechst 33342/
propidium iodide double staining, and an upregulated expression of
poly ADP-ribose polymerase was detected through western blotting. A disruption of the mitochondrial membrane potential was detected 2 h following
PDT. Significant suppression of cell migration and downregulation of
epidermal growth factor receptor (EGFR) expression were recorded following
PDT. These results indicate that the distribution of
photosensitizer leads to differences in the generation of ROS, which subsequently determines the type of cell death. Overall, mitochondrial activation under oxidative stress is important in the 9-HPbD-PDT-induced apoptosis of
HN-3 cells. Migration suppression of
HN-3 cells following
PDT may be associated with the inhibited expression of EGFR, due to oxidative stress.