Paradoxical effect of rosmarinic acid on metastatic melanoma B16F10 cells

2013 ◽  
Vol 18 ◽  
pp. S388-S389
Author(s):  
A. Olivares ◽  
D. Achel ◽  
M. Alcaraz ◽  
E. Olmos ◽  
M. Alcaraz-saura ◽  
...  
Keyword(s):  
Metastatic Melanoma ◽  
Rosmarinic Acid ◽  
Paradoxical Effect ◽  
B16f10 Cells ◽  
Melanoma B16f10

scholarly journals Effect of Rosmarinic Acid and Ionizing Radiation on Glutathione in Melanoma B16F10 Cells: A Translational Opportunity

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1291
Author(s):  
Amparo Olivares ◽  
Miguel Alcaraz-Saura ◽  
Daniel Gyingiri Achel ◽  
Miguel Alcaraz
Keyword(s):  
Oxidative Stress ◽  
Ionizing Radiation ◽  
Metabolic Pathway ◽  
Rosmarinic Acid ◽  
Cell Damage ◽  
Oxidized Glutathione ◽  
B16f10 Cells ◽  
Prostate Epithelial Cells ◽  
Significant Damage ◽  
Melanoma B16f10

To explain a paradoxical radiosensitizing effect of rosmarinic acid (RA) on the melanoma B16F10 cells, we analyzed the glutathione (GSH) intracellular production on this cell (traditionally considered radioresistant) in comparison with human prostate epithelial cells (PNT2) (considered to be radiosensitive). In PNT2 cells, the administration of RA increased the total GSH content during the first 3 h (p < 0.01) as well as increased the GSH/oxidized glutathione (GSSG) ratio in all irradiated cultures during all periods studied (1h and 3h) (p < 0.001), portraying an increase in the radioprotective capacity. However, in B16F10 cells, administration of RA had no effect on the total intracellular GSH levels, decreasing the GSH/GSSG ratio (p < 0.01); in addition, it caused a significant reduction in the GSH/GSSG ratio in irradiated cells (p < 0.001), an expression of radioinduced cell damage. In B16F10 cells, the administration of RA possibly activates the metabolic pathway of eumelanin synthesis that would consume intracellular GSH, thereby reducing its possible use as a protector against oxidative stress. The administration of this type of substance during radiotherapy could potentially protect healthy cells for which RA is a powerful radioprotector, and at the same time, cause significant damage to melanoma cells for which it could act as a radiosensitive agent.

Treatment of Metastatic Melanoma B16F10 by the Flavonoids Tangeretin, Rutin, and Diosmin

2005 ◽  
Vol 53 (17) ◽  
pp. 6791-6797 ◽  
Author(s):  
Cristina Martínez Conesa ◽  
Vicente Vicente Ortega ◽  
M. Josefa Yáñez Gascón ◽  
Miguel Alcaraz Baños ◽  
Manuel Canteras Jordana ◽  
...  
Keyword(s):  
Metastatic Melanoma ◽  
Melanoma B16f10

scholarly journals Unveiling the Differential Antioxidant Activity of Maslinic Acid in Murine Melanoma Cells and in Rat Embryonic Healthy Cells Following Treatment with Hydrogen Peroxide

Molecules ◽  
2020 ◽  
Vol 25 (17) ◽  
pp. 4020
Author(s):  
Khalida Mokhtari ◽  
Amalia Pérez-Jiménez ◽  
Leticia García-Salguero ◽  
José A. Lupiáñez ◽  
Eva E. Rufino-Palomares
Keyword(s):  
Antioxidant Enzyme ◽  
Cell Lines ◽  
Enzyme Activities ◽  
Biological Properties ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Glutathione S Transferase ◽  
Maslinic Acid ◽  
B16f10 Cells ◽  
Melanoma B16f10

Maslinic acid (MA) is a natural triterpene from Olea europaea L. with multiple biological properties. The aim of the present study was to examine MA’s effect on cell viability (by the MTT assay), reactive oxygen species (ROS levels, by flow cytometry) and key antioxidant enzyme activities (by spectrophotometry) in murine skin melanoma (B16F10) cells compared to those on healthy cells (A10). MA induced cytotoxic effects in cancer cells (IC50 42 µM), whereas no effect was found in A10 cells treated with MA (up to 210 µM). In order to produce a stress situation in cells, 0.15 mM H2O2 was added. Under stressful conditions, MA protected both cell lines against oxidative damage, decreasing intracellular ROS, which were higher in B16F10 than in A10 cells. The treatment with H2O2 and without MA produced different responses in antioxidant enzyme activities depending on the cell line. In A10 cells, all the enzymes were up-regulated, but in B16F10 cells, only superoxide dismutase, glutathione S-transferase and glutathione peroxidase increased their activities. MA restored the enzyme activities to levels similar to those in the control group in both cell lines, highlighting that in A10 cells, the highest MA doses induced values lower than control. Overall, these findings demonstrate the great antioxidant capacity of MA.

Effect of downregulation of ZEB1 on vimentin expression, tumour migration and tumourigenicity of melanoma B16F10 cells and CSCs

2014 ◽  
Vol 38 (4) ◽  
pp. 452-461 ◽  
Author(s):  
Jun Dou ◽  
Xiangfeng He ◽  
Yurong Liu ◽  
Yaqian Wang ◽  
Fengshu Zhao ◽  
...  
Keyword(s):  
Vimentin Expression ◽  
B16f10 Cells ◽  
Melanoma B16f10

scholarly journals Jolkinolide B induces apoptosis and inhibits tumor growth in mouse melanoma B16F10 cells by altering glycolysis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Caixia Gao ◽  
Xinyan Yan ◽  
Bo Wang ◽  
Lina Yu ◽  
Jichun Han ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Mouse Melanoma ◽  
B16f10 Cells ◽  
Melanoma B16f10

scholarly journals Anti-metastatic Effect of Garlic Hexane Extract on Lung Metastasis Induced by Melanoma B16F10 Cells in Mice

2016 ◽  
Vol 26 (2) ◽  
pp. 259-264
Author(s):  
Min Jung Ko ◽  
Seetharaman Rajasekar ◽  
Ziyu Wang ◽  
Mei Li ◽  
Jung Ho Kwak ◽  
...  
Keyword(s):  
Lung Metastasis ◽  
Hexane Extract ◽  
B16f10 Cells ◽  
Melanoma B16f10

scholarly journals Graphene-Induced Hyperthermia (GIHT) Combined With Radiotherapy Fosters Immunogenic Cell Death

2021 ◽  
Vol 11 ◽  
Author(s):  
Malgorzata J. Podolska ◽  
Xiaomei Shan ◽  
Christina Janko ◽  
Rabah Boukherroub ◽  
Udo S. Gaipl ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Combined Treatment ◽  
Infrared Light ◽  
Immunogenic Cell Death ◽  
Tumor Cell Death ◽  
Induced Hyperthermia ◽  
B16f10 Cells ◽  
Melanoma B16f10

Radiotherapy and chemotherapy are the standard interventions for cancer patients, although cancer cells often develop radio- and/or chemoresistance. Hyperthermia reduces tumor resistance and induces immune responses resulting in a better prognosis. We have previously described a method to induce tumor cell death by local hyperthermia employing pegylated reduced graphene oxide nanosheets and near infrared light (graphene-induced hyperthermia, GIHT). The spatiotemporal exposure/release of heat shock proteins (HSP), high group mobility box 1 protein (HMGB1), and adenosine triphosphate (ATP) are reported key inducers of immunogenic cell death (ICD). We hypothesize that GIHT decisively contributes to induce ICD in irradiated melanoma B16F10 cells, especially in combination with radiotherapy. Therefore, we investigated the immunogenicity of GIHT alone or in combination with radiotherapy in melanoma B16F10 cells. Tumor cell death in vitro revealed features of apoptosis that is progressing fast into secondary necrosis. Both HSP70 and HMGB1/DNA complexes were detected 18 hours post GIHT treatment, whereas the simultaneous release of ATP and HMGB1/DNA was observed only 24 hours post combined treatment. We further confirmed the adjuvant potential of these released DAMPs by immunization/challenge experiments. The inoculation of supernatants of cells exposed to sole GIHT resulted in tumor growth at the site of inoculation. The immunization with cells exposed to sole radiotherapy rather fostered the growth of secondary tumors in vivo. Contrarily, a discreet reduction of secondary tumor volumes was observed in mice immunized with a single dose of cells and supernatants treated with the combination of GIHT and irradiation. We propose the simultaneous release of several DAMPs as a potential mechanism fostering anti-tumor immunity against previously irradiated cancer cells.

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