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.

中文翻译：

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光动力疗法通过活性氧调节癌症干细胞的命运。

光动力疗法（PDT）是一种有效且有前景的癌症治疗方法。PDT通过光化学反应直接产生活性氧（ROS）。这种氧依赖性外源ROS具有抗癌干细胞（CSC）作用。此外，PDT 还可能通过改变代谢、内质网应激或线粒体膜电位来增加 ROS 的产生。众所周知，PDT中ROS的半衰期短，反应活性高，扩散距离有限。因此，PDT的主要靶向位置往往是光敏剂的亚细胞定位，这有助于我们解释PDT如何影响CSC特征，包括分化、自我更新、凋亡、自噬和免疫原性。一般来说，过量的ROS会损害氧化还原系统，对DNA等分子造成氧化损伤，改变线粒体通透性，激活未折叠蛋白反应、自噬和CSC静息状态。因此，了解ROS影响CSC的分子机制有利于提高PDT效率，预防肿瘤复发和转移。在本文中，我们回顾了两种类型的光化学反应对PDT的影响、代谢过程以及不同亚细胞位置的ROS对CSC的生物学效应。