Photosensitized rose Bengal-induced phototoxicity on human melanoma cell line under natural sunlight exposure

Srivastav, Ajeet K.; Mujtaba, Syed Faiz; Dwivedi, Ashish; Amar, Saroj Kumar; Goyal, Shruti; Verma, Ankit; Kushwaha, Hari Narayan; Chaturvedi, Rajnish Kumar; Ray, Ratan Singh

doi:10.1016/j.jphotobiol.2015.12.001

Cited by 25 publications

(15 citation statements)

References 30 publications

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“…Mitochondrial depolarization was observed in A375 cells treated with Ketoprofen and UVB light [ 73 ]. Treatment with Rose Bengal, followed by UVB and UVA exposures also led to decrease in mitochondrial membrane potential as well as translocation of phosphatidylserine from inner to outer plasma membrane in A375 cells [ 80 ]. Decrease in mitochondrial membrane potential can be visualized from the decrease in fluorescence intensity from cells bound to JC-1 and also quantified through flow cytometry.…”

Section: Resultsmentioning

confidence: 99%

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9-phenyl acridine photosensitizes A375 cells to UVA radiation

Hansda

Ghosh

2020

Heliyon

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Acridines are an important class of bioactive molecules having varied uses. Its derivative, 9-phenylacridine (ACPH) had been found to exhibit antitumor activity both in cell lines and in vivo model. Its DNA binding ability and absorbance in the ultraviolet range encouraged us to investigate its role as a photosensitizer with UVA radiation. We investigated the effects of ACPH prior to UVA exposure on in vitro DNA through photo-cleavage assay. Effect of such treatment was also studied in cultured A375 melanoma cells. Endpoints studied included morphological changes, evaluation of cellular viability, scratch assay, intracellular reactive oxygen species (ROS) production, DNA damage, lipid peroxidation, glutathione (GSH) level, autophagy, cell cycle progression, depletion of mitochondrial membrane potential (ΔΨmt), induction of apoptosis and Hoechst dye efflux assay. Our findings indicated that ACPH could sensitize damage to DNA induced by UVA both in vitro and in cells. It could also potentiate cell killing by UVA. It arrested cells in G 2 /M phase and induced apoptotic death through mitochondria mediated pathway. This sensitization was through enhancement of intracellular ROS. Our findings also indicated that the stem cells side population was reduced on such treatment. The findings are important as it indicates ACPH as a promising photosensitizer and indicates its possible role in photodynamic therapy.

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Section: Resultsmentioning

confidence: 99%

“…Ketoprofen and mefloquine with UVB too, upregulated Bax in HaCaT cells [ 73 , 74 ]. Rose Bengal followed by UVB and UVA exposures increased the Bax expression to induce apoptotic cell death in A375 cells [ 80 ]. We had checked the expression of Bax after pretreatment with ACPH (2 μM) on UVA (15 KJ/m 2 ) exposure.…”

Section: Resultsmentioning

confidence: 99%

9-phenyl acridine photosensitizes A375 cells to UVA radiation

Hansda

Ghosh

2020

Heliyon

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“…The apoptosis initiation is confirmed by this process and result. Phosphatidylserine is transported inside the lipid bilayer by the Mg‐ATP‐dependent enzyme, amino‐phospholipid translocase . Annexin V is Ca +2 dependent phosphatidylserine binding dye used for early stage of apoptotic detection.…”

Section: Discussionmentioning

confidence: 99%

“…Phosphatidylserine is transported inside the lipid bilayer by the Mg-ATPdependent enzyme, amino-phospholipid translocase. 60 Annexin V is Ca +2 dependent phosphatidylserine binding dye used for early stage of apoptotic detection. Propidium iodide is membrane impermeant dye used for cell viability.…”

Section: Discussionmentioning

confidence: 99%

Biochemical regulation and structural analysis of copper‐transporting ATPase in a human hepatoma cell line for Wilson disease

Agnihotry

Dhusia

Srivastav

et al. 2019

J of Cellular Biochemistry

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Hepatic copper levels differ among patients with Wilson disease (WD) and normal individuals depending on the dietary intake, copper bioavailability, and genetic factors. Copper chloride (CuCl2) caused dose‐dependent reduction in cell viability of human teratocarcinoma (HepG2) cell line, measured using the 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Cells were exposed to different concentrations of CuCl2 in log doses and maximum cell viability reduction was recorded at 15 µg/mL. Toxic dose of CuCl2 is potent inducer of reactive oxygen species (ROS). Apoptosis as a pattern of cell death was confirmed through sub‐G1 fraction and morphological changes such as mitochondrial depolarization, endoplasmic reticulum and lysosomal destabilization, phosphatidylserine translocation, and DNA damage. Our transcriptional and translational results strongly support apoptotic cell death. Using the available data present in dbSNP and bioinformatics tools, three nonsynonymous single nucleotide polymorphisms (nsSNPs) were identified as deleterious, reducing the stability of protein ATP7B. Structural analysis of native and mutant ATP7B proteins was investigated using molecular dynamics simulation (MDS) approach. Mutation in ATP7B gene might disturb the structural conformation and catalytic function of the ATP7B protein may be inducing WD. Hence, excess dietary intake of copper chloride must be avoided for safety of health to prevent from WD.

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“…Importantly, examination of the serum of metastatic melanoma patients treated with intralesional PV-10 revealed significantly higher levels of HMGB1 post-treatment compared to pre-treatment [112], indicating a systemic immunogenic response. Interestingly, when the photosensitized dye is applied to melanoma cells and exposed to natural sunlight, cell death occurs via increased oxidative stress inducing p53-mediated apoptosis [114]. Whether this suggests exposure of lesions to natural sunlight post-treatment would be beneficial to patients is unclear.…”

Section: Rose Bengalmentioning

confidence: 99%

Insights into the Molecular Mechanisms Behind Intralesional Immunotherapies for Advanced Melanoma

Vidovic

Giacomantonio

2020

Cancers

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The incidence of cutaneous melanoma, a highly malignant skin cancer, is increasing yearly. While surgical removal of the tumor is the mainstay of treatment for patients with locally confined disease, those with metastases face uncertainty when it comes to their treatment. As melanoma is a relatively immunogenic cancer, current guidelines suggest using immunotherapies that can rewire the host immune response to target melanoma tumor cells. Intralesional therapy, where immunomodulatory agents are injected directly into the tumor, are an emerging aspect of treatment for in-transit melanoma because of their ability to mitigate severe off-target immune-related adverse events. However, their immunomodulatory mechanisms are poorly understood. In this review, we will summarize and discuss the different intralesional therapies for metastatic melanoma with respect to their clinical outcomes and immune molecular mechanisms.

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Photosensitized rose Bengal-induced phototoxicity on human melanoma cell line under natural sunlight exposure

Cited by 25 publications

References 30 publications

9-phenyl acridine photosensitizes A375 cells to UVA radiation

9-phenyl acridine photosensitizes A375 cells to UVA radiation

Biochemical regulation and structural analysis of copper‐transporting ATPase in a human hepatoma cell line for Wilson disease

Insights into the Molecular Mechanisms Behind Intralesional Immunotherapies for Advanced Melanoma

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