Abstract
Photodynamic therapy (PDT) is an emerging cancer therapy that uses the combination of non-toxic dyes or photosensitizers (PS) and harmless visible light to produce reactive oxygen species and destroy tumors. The PS can be localized in various organelles such as mitochondria, lysosomes, endoplasmic reticulum, Golgi apparatus and plasma membranes and this sub-cellular location governs much of the signaling that occurs after PDT. There is an acute stress response that leads to changes in calcium and lipid metabolism and causes the production of cytokines and stress response mediators. Enzymes (particularly protein kinases) are activated and transcription factors are expressed. Many of the cellular responses center on mitochondria and frequently lead to induction of apoptosis by the mitochondrial pathway involving caspase activation and release of cytochrome c. Certain specific proteins (such as Bcl-2) are damaged by PDT-induced oxidation thereby increasing apoptosis, and a build-up of oxidized proteins leads to an ER-stress response that may be increased by proteasome inhibition. Autophagy plays a role in either inhibiting or enhancing cell death after PDT.
Highlights
Photodynamic therapy (PDT) is a promising therapeutic procedure for the management of a variety of solid tumors and non-malignant lesions
Chiu et al [60,61] indicated that commitment to cell death after PDT occurs prior to Bax activation while Usuada et al [62] reported that Smac/DIABLO promotes apoptosis after Pc4-PDT in a Bax dependent manner
Using an overexpression model in LNcaP cells they found that Etk/Bmx is an effector of PI3-kinase and that the PI3-kinase/Etk pathway is involved in the protection of prostate carcinoma cells from apoptosis in response to PDT
Summary
Photodynamic therapy (PDT) is a promising therapeutic procedure for the management of a variety of solid tumors and non-malignant lesions. The anticancer effect of PDT is a consequence of a lowto-moderately selective degree of photosensitizer (PS) uptake by proliferating malignant cells, direct cytotoxicity of reactive oxygen species (ROS) and a severe vascular damage that impairs blood supply to the treated area [6,7]. Those biological effects of PDT are limited to the particular areas of tissues exposed to light. In the present review we aim to describe and summarize different cell death pathways activated by PDT [16,17] and describe the key players controlling cell death related to PDT (Table 1)
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