Mossakowska Beata, Fabisiewicz Anna, Siedlecki Janusz
Zakład Onkologii Molekularnej i Translacyjnej Narodowy, Instytut Onkologii im. Marii Skłodowskiej-Curie - Państwowy Instytut Badawczy, Roentgena 5, 02-781 Warszawa.
Zakład Onkologii Molekularnej i Translacyjnej Narodowy Instytut Onkologii im. Marii Skłodowskiej-Curie - Państwowy Instytut Badawczy ul. Roentgena 5, 02-781 Warszawa.
Postepy Biochem. 2021 Jul 19;67(3):236-247. doi: 10.18388/pb.2021_394. Print 2021 Sep 30.
Photodynamic therapy (PDT) is one of the least toxic methods causing the death of cancer cells. Photosensitizer (PS) applied to a patient accumulates in the tumor, where under the appropriate wavelength and insensitivity of light is activated. Activated PS in the presence of oxygen produces reactive oxygen species (ROS), which make significant damage leading to the destruction of cancer cells by apoptosis, necrosis or autophagic process. Moreover, PDT causes an acute local inflammatory response that is involved in removing dead cells, restoring normal tissue homeostasis, and sometimes leads to the development of systemic immunity. However, some cells may survive treatment and develop resistance. Mechanisms, which lead to decrease of the level of PS in cells may be involved in the cytoprotection of cancer cells from PDT. Furthermore, increased activity of antioxidant mechanisms, overexpression of molecular chaperones and activation of survival pathways can protect cells from PDT.
光动力疗法(PDT)是导致癌细胞死亡的毒性最小的方法之一。应用于患者的光敏剂(PS)在肿瘤中蓄积,在适当波长和光照下被激活。激活的PS在有氧存在的情况下产生活性氧(ROS),ROS造成严重损伤,通过凋亡、坏死或自噬过程导致癌细胞破坏。此外,PDT引起急性局部炎症反应,该反应参与清除死亡细胞、恢复正常组织稳态,有时还会导致全身免疫的发展。然而,一些细胞可能在治疗后存活并产生耐药性。导致细胞内PS水平降低的机制可能参与癌细胞对PDT的细胞保护作用。此外,抗氧化机制活性增加、分子伴侣过度表达和生存途径激活可保护细胞免受PDT损伤。