Published online Jul 26, 2020. doi: 10.4252/wjsc.v12.i7.562
Peer-review started: February 26, 2020
First decision: April 25, 2020
Revised: May 17, 2020
Accepted: May 21, 2020
Article in press: May 21, 2020
Published online: July 26, 2020
Photodynamic therapy (PDT) is an effective and promising cancer treatment. PDT directly generates reactive oxygen species (ROS) through photochemical reactions. This oxygen-dependent exogenous ROS has anti-cancer stem cell (CSC) effect. In addition, PDT may also increase ROS production by altering metabolism, endoplasmic reticulum stress, or potential of mitochondrial membrane. It is known that the half-life of ROS in PDT is short, with high reactivity and limited diffusion distance. Therefore, the main targeting position of PDT is often the subcellular localization of photosensitizers, which is helpful for us to explain how PDT affects CSC characteristics, including differentiation, self-renewal, apoptosis, autophagy, and immunogenicity. Broadly speaking, excess ROS will damage the redox system and cause oxidative damage to molecules such as DNA, change mitochondrial permeability, activate unfolded protein response, autophagy, and CSC resting state. Therefore, understanding the molecular mechanism by which ROS affect CSCs is beneficial to improve the efficiency of PDT and prevent tumor recurrence and metastasis. In this article, we review the effects of two types of photochemical reactions on PDT, the metabolic processes, and the biological effects of ROS in different subcellular locations on CSCs.
Core tip: Photodynamic therapy (PDT) is an effective and promising cancer treatment. PDT directly produces reactive oxygen species (ROS) through photochemical reactions. In this article, we review the production process of oxygen-dependent exogenous ROS and the possible endogenous ROS generation process after PDT-mediated subcellular organelle stress. The intracellular metabolism of several ROS produced by PDT is analyzed. Given the extremely short half-life and limited diffusion distance of ROS, we explain from the subcellular localization of photosensitizers how PDT affects the characteristics of cancer stem cells through changes in mitochondrial permeability, activation of unfolded protein responses, autophagy and so on.