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 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 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.

scholarly journals Green Synthesis of Zinc Oxide Nanoparticles via Algal Route and its Action on Cancerous Cells and Pathogenic Microbes

2020 ◽  
Vol 3 (1) ◽  
pp. 15-27
Author(s):  
Priyankari Bhattacharya ◽  
Kasturi Chatterjee ◽  
Snehasikta Swarnakar ◽  
Sathi Banerjee
Keyword(s):  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Metal Oxide Nanoparticles ◽  
Melanoma Cells ◽  
Oxide Nanoparticles ◽  
Cellular Viability ◽  
Zno Nps ◽  
B16f10 Cells ◽  
Melanoma B16f10 ◽  
Minimal Damage

Application of metal oxide nanoparticles for treatment of melanoma cells and microbes is being investigated. Zinc oxide nanoparticles (ZnO NPs) deserve special mention where particles cause destruction of melanoma cells with minimal damage to healthy cells. In the present study, pure phase ZnO NPs with particle size of 3.1 nm were synthesized by green route using algal extract. Skin melanoma (B16F10) cells were treated with synthesized ZnO NP and compared with commercial ZnO NPs and analysed for ED50 for cellular viability using 3% (w/v) of the doses. Sensitivity of B16F10 cells towards green synthesized ZnO NP was found to be more than commercial ZnO NPs. Results showed greater reduction in viability of cells exposed to green synthesized ZnO NPs and with increasing dose of the ZnO NPs, percentage viability of cells gradually reduced. 50% decrease in cellular viability (ED50) was obtained for green synthesized ZnO NP at 3% dose while commercial ZnO exhibited ED50 at 6% of doses. The ZnO NP also showed antimicrobial activity against Pseudomonas sp. and Staphylococcus sp. Zone of inhibition (ZOI) exhibited by Pseudomonas aeruginosa and Staphylococcus aureus for disc diffusion and well diffusion assay was around 10-22 mm and 9-12mm respectively.

Experimental Metastasis, Tumor Cell-Induced Coagulopathy and Primary Tumor Growth in Mice with Hemophilia A.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 725-725
Author(s):  
Florian Langer ◽  
Ali Amirkhosravi ◽  
Susan B. Ingersoll ◽  
Jamie M. Walker ◽  
Brigitte Spath ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Lung Metastasis ◽  
Hemophilia A ◽  
Lung Tumor ◽  
Tumor Biology ◽  
Thrombin Inhibitor ◽  
Hematogenous Metastasis ◽  
Intravascular Hemolysis ◽  
Clotting Factors ◽  
B16f10 Cells

Abstract During experimental lung metastasis, tumor cells adhere to the pulmonary microvasculature and activate coagulation via surface-expressed tissue factor (TF), leading to local fibrin deposition and platelet activation. This thrombotic microangiopathy, which facilitates tumor cell survival and extravasation, results in intravascular hemolysis and consumption of platelets and clotting factors. While interventional studies have demonstrated convincing efficacy of anticoagulants and anti-platelet agents in inhibiting metastasis, no information is available on how tumor biology may be affected by congenital bleeding disorders such as hemophilia A. We therefore used a syngeneic model of mouse melanoma to provide mechanistic insight into this area of uncertainty. By conventional RT-PCR, indirect flow cytometry using a novel polyclonal rabbit anti-mouse TF antibody, and one-stage clotting assays we detected strong expression of TF mRNA, antigen, and procoagulant activity in the murine B16F10 melanoma cell line. For metastasis experiments, control (n=17) and hemophilic mice (n=18), both on a mixed B6/129 background, were injected via the lateral tail vein with 2 x 105 B16F10 cells. After 18 days, macroscopic tumor nodules were counted on the lungs of sacrificed animals. Compared to controls (median 194, IQR 112–241), lung tumor formation was significantly reduced in mice with hemophilia A (100, 63–125; P<0.01). This genetic protection was completely reversed by a single dose of human FVIII (hFVIII) at 100 U/kg body weight 15 min prior to tumor cell injection (190, 156–300; n=10, P<0.001) and further pronounced by lepirudin (5 μg), a direct thrombin inhibitor (64, 58–73; n=7, P<0.05), suggesting that thrombin generation contributed to hematogenous metastasis in the absence of FVIII. Infusion of hFVIII into control mice (n=10) did not significantly alter the efficacy of melanoma lung seeding (P=0.35), although 50% of animals in this group showed confluent colony formation (>300 tumor nodules) as compared to 0% in the group pretreated with PBS. As expected, lepirudin significantly reduced numbers of pulmonary foci in control mice (96, 82–114; n=7, P<0.01). In these experiments, mortality was associated with metastatic tumor burden rather than with hemostatic competence of study mice. To assess tumor cell-induced coagulation activation in vivo, mice were injected intravenously with PBS (n=5 per group) or 1 x 106 B16F10 cells (n=10 per group). After 15 min, blood was collected by puncture of the retro-orbital plexus and analyzed for platelet count and plasma levels of FXa and hemoglobin, a sensitive marker of intravascular hemolysis. Consistent with our previous findings, injection of B16F10 cells evoked laboratory changes of consumptive coagulopathy in both groups of mice, with less pronounced changes in FVIII-deficient animals. Three weeks after subcutaneous implantation of 1 x 106 B16F10 cells into flanks of control and hemophilic mice (n=10 per group), there was a trend towards smaller tumor volumes in the latter group (5.2±3.4 cm3 vs. 9.4±5.3 cm3, P=0.08). Spontaneous lung metastasis was observed in 25% of control as compared to 0% of hemophilia A mice. Although strong TF expression by B16F10 cells may promote thrombin-dependent metastasis in mice with hemophilia A, amplification of coagulation by host FVIII appears to be necessary for maximum melanoma lung seeding.

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