scholarly journals Overview of Cell Death Mechanisms Induced by Rose Bengal Acetate-Photodynamic Therapy

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Elisa Panzarini ◽  
Valentina Inguscio ◽  
Luciana Dini
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Rose Bengal ◽  
Intracellular Localization ◽  
Photochemical Reactions ◽  
Ros Generation ◽  
Invasive Treatment ◽  
Rose Bengal Acetate ◽  
Efficient Induction ◽  
Apoptotic Pathways

Photodynamic Therapy (PDT) is a non-invasive treatment for different pathologies, cancer included, using three key components: non-toxic light-activated drug (Photosensitizer, PS), visible light, and oxygen. Their interaction triggers photochemical reactions leading to Reactive Oxygen Species (ROS) generation, that mediate cytotoxicity and cell death. In the present paper, the most important findings about the synthetic dye Rose Bengal Acetate (RBAc), an emerging photosensitizer for its efficient induction of cell death, will be reported with the aim to integrate RBAc phototoxicity to novel therapeutic PDT strategies against tumour cells. After its perinuclear intracellular localization, RBAc causes multiple subcellular organelles damage, that is, mitochondria, Endoplasmic Reticulum (ER), lysosomes, and Golgi complex. Indeed, RBAc exerts long-term phototoxicity through activation of both caspase-independent and- dependent apoptotic pathways and autophagic cell death. In particular, this latter cell death type may promote cell demise when apoptotic machinery is defective. The deep knowledge of RBAc photocytotoxicity will allow to better understand its potential photomedicine application in cancer.

Energy metabolism targeted drugs synergize with photodynamic therapy to potentiate breast cancer cell death

2014 ◽  
Vol 13 (12) ◽  
pp. 1793-1803 ◽  
Author(s):  
Xiaolan Feng ◽  
Yi Zhang ◽  
Pan Wang ◽  
Quanhong Liu ◽  
Xiaobing Wang
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Energy Metabolism ◽  
Combination Therapy ◽  
Breast Cancer Cells ◽  
Ros Generation ◽  
Targeted Drugs ◽  
Cancer Cell Death ◽  
Dependent Cell

Glycolytic inhibitors can synergistically enhance the photosensitivity of breast cancer cells by triggering cellular mitochondria- and caspase-dependent cell apoptosis, which was induced by additional ROS generation in combination therapy.

Enzyme-assisted photosensitization activates different apoptotic pathways in Rose Bengal acetate treated HeLa cells

2008 ◽  
Vol 131 (3) ◽  
pp. 391-399 ◽  
Author(s):  
Maria Grazia Bottone ◽  
Cristiana Soldani ◽  
Annunzia Fraschini ◽  
Anna Cleta Croce ◽  
Giovanni Bottiroli ◽  
...  
Keyword(s):  
Rose Bengal ◽  
Hela Cells ◽  
Rose Bengal Acetate ◽  
Apoptotic Pathways

scholarly journals PEGylated Purpurin 18 with Improved Solubility: Potent Compounds for Photodynamic Therapy of Cancer

Molecules ◽  
2019 ◽  
Vol 24 (24) ◽  
pp. 4477 ◽  
Author(s):  
Vladimíra Pavlíčková ◽  
Silvie Rimpelová ◽  
Michal Jurášek ◽  
Kamil Záruba ◽  
Jan Fähnrich ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Intracellular Localization ◽  
Zinc Ion ◽  
Cell Uptake ◽  
Oxygen Generation ◽  
Photodynamic Therapy Of Cancer ◽  
Predominant Type ◽  
Inhibitory Compound ◽  
Compound Concentration

Purpurin 18 derivatives with a polyethylene glycol (PEG) linker were synthesized as novel photosensitizers (PSs) with the goal of using them in photodynamic therapy (PDT) for cancer. These compounds, derived from a second-generation PS, exhibit absorption at long wavelengths; considerable singlet oxygen generation and, in contrast to purpurin 18, have higher hydrophilicity due to decreased logP. Together, these properties make them potentially ideal PSs. To verify this, we screened the developed compounds for cell uptake, intracellular localization, antitumor activity and induced cell death type. All of the tested compounds were taken up into cancer cells of various origin and localized in organelles known to be important PDT targets, specifically, mitochondria and the endoplasmic reticulum. The incorporation of a zinc ion and PEGylation significantly enhanced the photosensitizing efficacy, decreasing IC50 (half maximal inhibitory compound concentration) in HeLa cells by up to 170 times compared with the parental purpurin 18. At effective PDT concentrations, the predominant type of induced cell death was apoptosis. Overall, our results show that the PEGylated derivatives presented have significant potential as novel PSs with substantially augmented phototoxicity for application in the PDT of cervical, prostate, pancreatic and breast cancer.

In vitro and in vivo clearance of Rose Bengal Acetate-PhotoDynamic Therapy-induced autophagic and apoptotic cells

2013 ◽  
Vol 238 (7) ◽  
pp. 765-778 ◽  
Author(s):  
Elisa Panzarini ◽  
Valentina Inguscio ◽  
Bernardetta Anna Tenuzzo ◽  
Luciana Dini
Keyword(s):  
Photodynamic Therapy ◽  
Rose Bengal ◽  
Apoptotic Cells ◽  
Rose Bengal Acetate

scholarly journals Combination of photodynamic therapy (PDT) and anti-tumor immunity in cancer therapy

2018 ◽  
Vol 48 (2) ◽  
pp. 143-151 ◽  
Author(s):  
Hee Sook Hwang ◽  
Heejun Shin ◽  
Jieun Han ◽  
Kun Na
Keyword(s):  
Reactive Oxygen Species ◽  
Immune Response ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Adaptive Immune Response ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Tumor Cell Death ◽  
Target Sites

Abstract Photodynamic therapy (PDT) is performed using a photosensitizer and light of specific wavelength in the presence of oxygen to generate singlet oxygen and reactive oxygen species(ROS) in the cancer cells. The accumulated photosensitizers in target sites induce ROS generation upon light activation, then the generated cytotoxic reactive oxygen species lead to tumor cell death via apoptosis or necrosis, and damages the target sites which results tumor destruction. As a consequence, the PDT-mediated cell death is associated with anti-tumor immune response. In this paper, the effects of PDT and immune response on tumors are reviewed. Activation of an immune response regarding the innate and adaptive immune response, interaction with immune cells and tumor cells that associated with antitumor efficacy of PDT are also discussed.

scholarly journals Systemic MEK inhibition enhances the efficacy of 5-aminolevulinic acid-photodynamic therapy

2019 ◽  
Vol 121 (9) ◽  
pp. 758-767 ◽  
Author(s):  
Vipin Shankar Chelakkot ◽  
Jayoti Som ◽  
Ema Yoshioka ◽  
Chantel P. Rice ◽  
Suzette G. Rutihinda ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cancer Cells ◽  
Aminolevulinic Acid ◽  
Combined Therapy ◽  
Combined Treatment ◽  
Mek Inhibitor ◽  
Ros Generation ◽  
Strong Basis ◽  
Mek Inhibition

Abstract Background Protoporphyrin IX (PpIX) gets accumulated preferentially in 5-aminolevulinic acid (5-ALA)-treated cancer cells. Photodynamic therapy (PDT) utilises the accumulated PpIX to trigger cell death by light-induced generation of reactive oxygen species (ROS). We previously demonstrated that oncogenic Ras/MEK decreases PpIX accumulation in cancer cells. Here, we investigated whether combined therapy with a MEK inhibitor would improve 5-ALA-PDT efficacy. Methods Cancer cells and mice models of cancer were treated with 5-ALA-PDT, MEK inhibitor or both MEK inhibitor and 5-ALA-PDT, and treatment efficacies were evaluated. Results Ras/MEK negatively regulates the cellular sensitivity to 5-ALA-PDT as cancer cells pre-treated with a MEK inhibitor were killed more efficiently by 5-ALA-PDT. MEK inhibition promoted 5-ALA-PDT-induced ROS generation and programmed cell death. Furthermore, the combination of 5-ALA-PDT and a systemic MEK inhibitor significantly suppressed tumour growth compared with either monotherapy in mouse models of cancer. Remarkably, 44% of mice bearing human colon tumours showed a complete response with the combined treatment. Conclusion We demonstrate a novel strategy to promote 5-ALA-PDT efficacy by targeting a cell signalling pathway regulating its sensitivity. This preclinical study provides a strong basis for utilising MEK inhibitors, which are approved for treating cancers, to enhance 5-ALA-PDT efficacy in the clinic.

scholarly journals Connexin Hemichannel Activation by S-Nitrosoglutathione Synergizes Strongly with Photodynamic Therapy Potentiating Anti-Tumor Bystander Killing

Cancers ◽  
2021 ◽  
Vol 13 (20) ◽  
pp. 5062
Author(s):  
Chiara Nardin ◽  
Chiara Peres ◽  
Sabrina Putti ◽  
Tiziana Orsini ◽  
Claudia Colussi ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Atp Release ◽  
No Donor ◽  
Dorsal Skinfold Chamber ◽  
Endogenous Nitric Oxide ◽  
Bystander Killing ◽  
Apoptotic Pathways ◽  
Bystander Cell Death ◽  
Rapid Activation

In this study, we used B16-F10 cells grown in the dorsal skinfold chamber (DSC) preparation that allowed us to gain optical access to the processes triggered by photodynamic therapy (PDT). Partial irradiation of a photosensitized melanoma triggered cell death in non-irradiated tumor cells. Multiphoton intravital microscopy with genetically encoded fluorescence indicators revealed that bystander cell death was mediated by paracrine signaling due to adenosine triphosphate (ATP) release from connexin (Cx) hemichannels (HCs). Intercellular calcium (Ca2+) waves propagated from irradiated to bystander cells promoted intracellular Ca2+ transfer from the endoplasmic reticulum (ER) to mitochondria and rapid activation of apoptotic pathways. Combination treatment with S-nitrosoglutathione (GSNO), an endogenous nitric oxide (NO) donor that biases HCs towards the open state, greatly potentiated anti-tumor bystander killing via enhanced Ca2+ signaling, leading to a significant reduction of post-irradiation tumor mass. Our results demonstrate that HCs can be exploited to dramatically increase cytotoxic bystander effects and reveal a previously unappreciated role for HCs in tumor eradication promoted by PDT.

scholarly journals Rose Bengal Acetate photodynamic therapy-induced autophagy

2010 ◽  
Vol 10 (10) ◽  
pp. 1048-1055 ◽  
Author(s):  
Luciana Dini ◽  
Valentina Inguscio ◽  
Bernardetta Tenuzzo ◽  
Elisa Panzarini
Keyword(s):  
Photodynamic Therapy ◽  
Rose Bengal ◽  
Rose Bengal Acetate
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