Increased DNA repair capacity augments resistance of glioblastoma cells to photodynamic therapy

Ghahe, Somayeh Shahmoradi; Kosicki, Konrad; Wojewódzka, Maria; Majchrzak, Bartosz; Fogtman, Anna; Iwanicka-Nowicka, Roksana; Ciuba, Agata; Koblowska, Marta; Kruszewski, Marcin; Speina, Elżbieta

doi:10.1016/j.dnarep.2021.103136

Cited by 24 publications

(20 citation statements)

References 58 publications

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“…In this regard, a recent review by Aniogo and colleagues described in detail the possible molecular pathways that might be responsible for the escape of tumor cells from PDT [ 176 ]. Among the main mechanisms preventing the cytotoxic effects of PDT, the following elements might play an important role: (1) altered genetic profile, and particularly altered expression of tumor survival genes [ 177 – 179 ], (2) increase in DNA damage-repair processes [ 180 ], (3) increase in AKT/mTOR signaling, (4) expression of ROS-scavenger proteins (e.g., glutathione S-transferase (GST), glutathione peroxidase 4 (GPx4)) [ 181 , 182 ], and generation of nitric oxide (NO) [ 183 , 184 ]. Moreover, PDT can cause dysregulation of the antiapoptotic Bcl-2 protein at the mitochondrial membrane, overexpression of efflux proteins (e.g., P-glycoproteins), and formation of autolysosomes through recycling of cytoplasmic content for cell survival [ 176 , 185 ].…”

Section: Ferroptosismentioning

confidence: 99%

Which cell death modality wins the contest for photodynamic therapy of cancer?

et al. 2022

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Photodynamic therapy (PDT) was discovered more than 100 years ago. Since then, many protocols and agents for PDT have been proposed for the treatment of several types of cancer. Traditionally, cell death induced by PDT was categorized into three types: apoptosis, cell death associated with autophagy, and necrosis. However, with the discovery of several other regulated cell death modalities in recent years, it has become clear that this is a rather simple understanding of the mechanisms of action of PDT. New observations revealed that cancer cells exposed to PDT can pass through various non-conventional cell death pathways, such as paraptosis, parthanatos, mitotic catastrophe, pyroptosis, necroptosis, and ferroptosis. Nowadays, immunogenic cell death (ICD) has become one of the most promising ways to eradicate tumor cells by activation of the T-cell adaptive immune response and induction of long-term immunological memory. ICD can be triggered by many anti-cancer treatment methods, including PDT. In this review, we critically discuss recent findings on the non-conventional cell death mechanisms triggered by PDT. Next, we emphasize the role and contribution of ICD in these PDT-induced non-conventional cell death modalities. Finally, we discuss the obstacles and propose several areas of research that will help to overcome these challenges and lead to the development of highly effective anti-cancer therapy based on PDT.

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Section: Ferroptosismentioning

confidence: 99%

Which cell death modality wins the contest for photodynamic therapy of cancer?

et al. 2022

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“… 28 29 Therefore, this study conducted IHC analysis using 4-HNE, a second messenger in the ROS cascade, and 8-OhdG, which serves as a potential marker of DNA oxidation. 30 31 Additionally, the degree of apoptosis induction by each treatment was determined using Caspase-3 as a marker. 32 33 In consideration of the sufficient effect of treatment, the animals were sacrificed 3 days after the treatment.…”

Section: Discussionmentioning

confidence: 99%

Combined Effects of Focused Ultrasound and Photodynamic Treatment for Malignant Brain Tumors Using C6 Glioma Rat Model

et al. 2023

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Purpose Glioblastoma (GBM) is an intractable disease for which various treatments have been attempted, but with little effect. This study aimed to measure the effect of photodynamic therapy (PDT) and sonodynamic therapy (SDT), which are currently being used to treat brain tumors, as well as sono-photodynamic therapy (SPDT), which is the combination of these two. Materials and Methods Four groups of Sprague-Dawley rats were injected with C6 glioma cells in a cortical region and treated with PDT, SDT, and SPDT. Gd-MRI was monitored weekly and 18F-FDG-PET the day before and 1 week after the treatment. The acoustic power used during sonication was 5.5 W/cm 2 using a 0.5-MHz single-element transducer. The 633-nm laser was illuminated at 100 J/cm 2 . Oxidative stress and apoptosis markers were evaluated 3 days after treatment using immunohistochemistry (IHC): 4-HNE, 8-OhdG, and Caspase-3. Results A decrease in tumor volume was observed in MRI imaging 12 days after the treatment in the PDT group ( p <0.05), but the SDT group showed a slight increase compared to the 5-Ala group. The high expression rates of reactive oxygen species-related factors, such as 8-OhdG ( p <0.001) and Caspase-3 ( p <0.001), were observed in the SPDT group compared to other groups in IHC. Conclusion Our findings show that light with sensitizers can inhibit GBM growth, but not ultrasound. Although SPDT did not show the combined effect in MRI, high oxidative stress was observed in IHC. Further studies are needed to investigate the safety parameters to apply ultrasound in GBM.

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“…DNA oxidative damage and breaks can be mediated either directly via single-electron oxidation of DNA or indirectly by generation of O 2 − , HO·, and 1 O 2 [ 44 , 59 , 60 ]. Single-electron oxidation occurs when a Type I photosensitizer, in its excited triplet state, abstracts an electron/hydrogen atom from a DNA base.…”

Section: Reactive Oxygen Species Production and Mechanisms Of Actionmentioning

confidence: 99%

X-ray Activated Nanoplatforms for Deep Tissue Photodynamic Therapy

et al. 2023

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Photodynamic therapy (PDT), the use of light to excite photosensitive molecules whose electronic relaxation drives the production of highly cytotoxic reactive oxygen species (ROS), has proven an effective means of oncotherapy. However, its application has been severely constrained to superficial tissues and those readily accessed either endoscopically or laparoscopically, due to the intrinsic scattering and absorption of photons by intervening tissues. Recent advances in the design of nanoparticle-based X-ray scintillators and photosensitizers have enabled hybridization of these moieties into single nanocomposite particles. These nanoplatforms, when irradiated with diagnostic doses and energies of X-rays, produce large quantities of ROS and permit, for the first time, non-invasive deep tissue PDT of tumors with few of the therapeutic limitations or side effects of conventional PDT. In this review we examine the underlying principles and evolution of PDT: from its initial and still dominant use of light-activated, small molecule photosensitizers that passively accumulate in tumors, to its latest development of X-ray-activated, scintillator–photosensitizer hybrid nanoplatforms that actively target cancer biomarkers. Challenges and potential remedies for the clinical translation of these hybrid nanoplatforms and X-ray PDT are also presented.

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Increased DNA repair capacity augments resistance of glioblastoma cells to photodynamic therapy

Cited by 24 publications

References 58 publications

Which cell death modality wins the contest for photodynamic therapy of cancer?

Which cell death modality wins the contest for photodynamic therapy of cancer?

Combined Effects of Focused Ultrasound and Photodynamic Treatment for Malignant Brain Tumors Using C6 Glioma Rat Model

X-ray Activated Nanoplatforms for Deep Tissue Photodynamic Therapy

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