Effect of xanthohumol and 8-prenylnaringenin on MCF-7 breast cancer cells oxidative stress and mitochondrial complexes expression

2013 ◽  
Vol 114 (12) ◽  
pp. 2785-2794 ◽  
Author(s):  
M. Mar Blanquer-Rosselló ◽  
Jordi Oliver ◽  
Adamo Valle ◽  
Pilar Roca
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mitochondrial Complexes ◽  
Mcf 7

Oxidative Stress in Caffeine Action on the Proliferation and Death of Human Breast Cancer Cells MCF-7 and MDA-MB-231

2020 ◽  
pp. 1-11
Author(s):  
Kaliana Larissa Machado ◽  
Poliana Camila Marinello ◽  
Thamara Nishida Xavier Silva ◽  
Cássio Fernando Nunes Silva ◽  
Rodrigo Cabral Luiz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mcf 7

scholarly journals GPR91 Receptor Mediates Protection against Doxorubicin-Induced Cardiotoxicity without Altering Its Anticancer Efficacy. An In Vitro Study on H9C2 Cardiomyoblasts and Breast Cancer-Derived MCF-7 Cells

Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2177
Author(s):  
Matthieu Dallons ◽  
Esma Alpan ◽  
Corentin Schepkens ◽  
Vanessa Tagliatti ◽  
Jean-Marie Colet
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Protective Effect ◽  
Cancer Cells ◽  
1H Nmr ◽  
Breast Cancer Cells ◽  
Extracellular Fluid ◽  
H9c2 Cells ◽  
Experimental Conditions ◽  
Mcf 7

Doxorubicin (DOX) is an anticancer drug widely used in oncology, especially for breast cancer. The main limitation of DOX treatment is its cardiotoxicity due to the cumulative dose. Clinically, DOX-induced cardiomyopathy develops as a progressive heart failure caused by a progressive cardiomyocyte’s death. For long, the oxidative stress induced by DOX was considered as the main toxic mechanism responsible for heart damage, but it is now controverted, and other processes are investigated to develop cardioprotective strategies. Previously, we studied DOX-induced cardiotoxicity and dexrazoxane (DEX), the only cardioprotective compound authorized by the FDA, by 1H-NMR metabonomics in H9C2 cells. We observed an increased succinate secretion in the extracellular fluid of DEX-exposed cardiomyocytes, a finding that led us to the hypothesis of a possible protective role of this agonist of the GPR91 receptor. The objective of the present work was to study the effect of succinate (SUC) and cis-epoxysuccinate (cis-ES), two agonists of the GPR91 receptor, on DOX-induced cardiotoxicity to H9C2 cells. To this purpose, several toxicity parameters, including cell viability, oxidative stress and apoptosis, as well as the GPR91 expression, were measured to assess the effects of DEX, SUC and cis-ES either alone or in combination with DOX in H9C2 cells. A 1H-NMR-based metabonomic study was carried out on cellular fluids collected after 24 h to highlight the metabolic changes induced by those protective compounds. Moreover, the effects of each agonist given either alone or in combination with DOX were evaluated on MCF-7 breast cancer cells. GPR91 expression was confirmed in H9C2 cells, while no expression was found in MCF-7 cells. Under such experimental conditions, both SUC and cis-ES decreased partially the cellular mortality, the oxidative stress and the apoptosis induced by DOX. The SUC protective effect was similar to the DEX effect, but the protective effect of cis-ES was higher on oxidative stress and apoptosis. In addition, the metabonomics findings pointed out several metabolic pathways involved in the cardioprotective effects of both GPR91 agonists: the stimulation of aerobic metabolism with glucose as the main fuel, redox balance and phospholipids synthesis. Finally, none of the GPR91 agonists jeopardized the pharmacological effects of DOX on MCF-7 breast cancer cells.

Gold nanoparticles induced apoptosis via oxidative stress and mitochondrial dysfunctions in MCF‐7 breast cancer cells

2020 ◽  
Vol 35 (1) ◽  
Author(s):  
Elumalai Kowsalya ◽  
Kithiyon MosaChristas ◽  
Chinna Rani Inbaraj Jaquline ◽  
Pannerselvam Balashanmugam ◽  
Thiyagarajan Devasena
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Gold Nanoparticles ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mitochondrial Dysfunctions ◽  
Induced Apoptosis ◽  
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scholarly journals Metformin Induces Apoptosis and Cell Cycle Arrest Mediated by Oxidative Stress, AMPK and FOXO3a in MCF-7 Breast Cancer Cells

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e98207 ◽  
Author(s):  
Eveline A. I. F. Queiroz ◽  
Stephanie Puukila ◽  
Rosangela Eichler ◽  
Sandra C. Sampaio ◽  
Heidi L. Forsyth ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cycle Arrest ◽  
Mcf 7

scholarly journals Effects of Quercetin-Loaded Nanoparticles on MCF-7 Human Breast Cancer Cells

Medicina ◽  
2019 ◽  
Vol 55 (4) ◽  
pp. 114 ◽  
Author(s):  
Firoozeh Niazvand ◽  
Mahmoud Orazizadeh ◽  
Layasadat Khorsandi ◽  
Mohammadreza Abbaspour ◽  
Esrafil Mansouri ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Toxic Effect ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cell Line Cell ◽  
Mcf 7

Background and objectives: Previous studies have shown anti-tumor activity of quercetin (QT). However, the low bioavailability of QT has restricted its use. This study aimed to assess the toxic effect of QT encapsulated in solid lipid nanoparticles (QT-SLNs) on the growth of MCF-7 human breast cancer cells. Materials and Methods: MCF-7 and MCF-10A (non-tumorigenic cell line) cell lines treated with 25 µmol/mL of QT or QT-SLNs for 48 h. Cell viability, colony formation, oxidative stress, and apoptosis were evaluated to determine the toxic effects of the QT-SLNs. Results: The QT-SLNs with appropriate characteristics (particle size of 85.5 nm, a zeta potential of −22.5 and encapsulation efficiency of 97.6%) were prepared. The QT-SLNs showed sustained QT release until 48 h. Cytotoxicity assessments indicated that QT-SLNs inhibited MCF-7 cells growth with a low IC50 (50% inhibitory concentration) value, compared to the free QT. QT-SLNs induced a significant decrease in the viability and proliferation of MCF-7 cells, compared to the free QT. QT-SLN significantly increased reactive oxygen species (ROS) level and MDA contents and significantly decreased antioxidant enzyme activity in the MCF-7 cells. Following QT-SLNs treatment, the expression of the Bcl-2 protein significantly decreased, whereas Bx expression showed a significant increase in comparison with free QT-treated cells. Furthermore, The QT-SLNs significantly increased apoptotic and necrotic indexes in MCF-7 cells. Viability, proliferation, oxidative stress and apoptosis of MCF-10A cells were not affected by QT or QT-SLNs. Conclusions: According to the results of this study, SLN significantly enhanced the toxic effect of QT against human breast cancer cells.

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