scholarly journals Molecular Mechanisms of Polybrominated Diphenyl Ethers (BDE-47, BDE-100, and BDE-153) in Human Breast Cancer Cells and Patient-Derived Xenografts

2019 ◽  
Vol 169 (2) ◽  
pp. 380-398 ◽  
Author(s):  
Noriko Kanaya ◽  
Lauren Bernal ◽  
Gregory Chang ◽  
Takuro Yamamoto ◽  
Duc Nguyen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Polybrominated Diphenyl Ethers ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Diphenyl Ethers

scholarly journals Structural and Molecular Mechanisms of Cytokine-Mediated Endocrine Resistance in Human Breast Cancer Cells

2017 ◽  
Vol 65 (6) ◽  
pp. 1122-1135.e5 ◽  
Author(s):  
Joshua D. Stender ◽  
Jerome C. Nwachukwu ◽  
Irida Kastrati ◽  
Yohan Kim ◽  
Tobias Strid ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Endocrine Resistance ◽  
Human Breast Cancer Cells ◽  
Human Breast

Unveiling the molecular mechanisms involved in the cytotoxicity induced by photodynamic therapy in human breast cancer cells

2015 ◽  
Vol 12 (3) ◽  
pp. 349
Author(s):  
A.F. dos Santos ◽  
L.F. Terra ◽  
R.A.M. Wailemann ◽  
T.C. Oliveira ◽  
M.S. Baptista ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Photodynamic Therapy ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Human Breast Cancer Cells ◽  
Human Breast

scholarly journals Distinct photooxidation-induced cell death pathways lead to selective killing of human breast cancer cells

2020 ◽  
Author(s):  
Ancély F. dos Santos ◽  
Alex Inague ◽  
Gabriel S. Arini ◽  
Letícia F. Terra ◽  
Rosangela A.M. Wailemann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Cell Death Pathways ◽  
Photooxidative Damage ◽  
Tumorigenic Cells

AbstractLack of effective treatments for aggressive breast cancer is still a major global health problem. We previously reported that Photodynamic Therapy using Methylene Blue as photosensitizer (MB-PDT) massively kills metastatic human breast cancer, marginally affecting healthy cells. In this study we aimed to unveil the molecular mechanisms behind MB-PDT effectiveness. Through lipidomic and biochemical approaches we demonstrated that MB-PDT efficiency and specificity relies on polyunsaturated fatty acids-enriched membranes and on the better capacity to deal with photooxidative damage displayed by non-tumorigenic cells. We found out that, in tumorigenic cells, lysosome membrane permeabilization is accompanied by ferroptosis and/or necroptosis. Our results broadened the understanding of MB-PDT-induced photooxidation mechanisms and specificity in breast cancer cells. Therefore, we demonstrated that efficient approaches could be designed on the basis of lipid composition and metabolic features for hard-to-treat cancers. The results further reinforce MB-PDT as a therapeutic strategy for highly aggressive human breast cancer cells.

scholarly journals Distinct photo-oxidation-induced cell death pathways lead to selective killing of human breast cancer cells

2020 ◽  
Vol 11 (12) ◽  
Author(s):  
Ancély F. Dos Santos ◽  
Alex Inague ◽  
Gabriel S. Arini ◽  
Letícia F. Terra ◽  
Rosangela A. M. Wailemann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Photo Oxidation ◽  
Tumorigenic Cells

AbstractLack of effective treatments for aggressive breast cancer is still a major global health problem. We have previously reported that photodynamic therapy using methylene blue as photosensitizer (MB-PDT) massively kills metastatic human breast cancer, marginally affecting healthy cells. In this study, we aimed to unveil the molecular mechanisms behind MB-PDT effectiveness and specificity towards tumor cells. Through lipidomics and biochemical approaches, we demonstrated that MB-PDT efficiency and specificity rely on polyunsaturated fatty acid-enriched membranes and on the better capacity to deal with photo-oxidative damage displayed by non-tumorigenic cells. We found out that, in tumorigenic cells, lysosome membrane permeabilization is accompanied by ferroptosis and/or necroptosis. Our results also pointed at a cross-talk between lysosome-dependent cell death (LDCD) and necroptosis induction after photo-oxidation, and contributed to broaden the understanding of MB-PDT-induced mechanisms and specificity in breast cancer cells. Therefore, we demonstrated that efficient approaches could be designed on the basis of lipid composition and metabolic features for hard-to-treat cancers. The results further reinforce MB-PDT as a therapeutic strategy for highly aggressive human breast cancer cells.

Molecular mechanisms of oestrogen action on growth of human breast cancer cells in culture

2012 ◽  
Vol 9 (1) ◽  
Author(s):  
Philippa D. Darbre
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Oestrogen Receptor ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Signalling Pathways ◽  
Human Breast Cancer Cells ◽  
Human Breast

AbstractGrowth responses to oestrogen can be reproducibly obtained using a selection of oestrogen-receptor-containing human breast cancer cell lines, and molecular mechanisms have been shown to include modulation to growth factor/receptor/signalling pathways, cell-cycle proteins, apoptosis, differentiation, adhesion, motility and migration. Considerable progress has been made in understanding the molecular basis of oestrogen action on gene expression through the ligand-activated transcription factors human oestrogen receptor α (ERα) and ERβ and the resulting effects on global gene expression patterns, but the full profile of coordination of the alterations, which brings about changes in cell growth through genomic and non-genomic mechanisms remain to be fully elucidated. Oestrogen regulation of cell growth involves a complex cross-talk between oestrogen receptor and growth factor signalling pathways such that inhibition of one pathway may lead to stimulation of another, which may explain the remarkable ability of human breast cancer cells to escape from any mode of imposed growth inhibition be it oestrogen deprivation or administration of antioestrogen. Although studies on cell growth have focused to date on the effects of physiological oestrogens, many hundreds of environmental chemicals with oestrogenic properties have now been measured in the human breast. Whether or not the weight of evidence eventually establishes any causal link of complex mixtures of environmental oestrogenic chemicals with breast cancer, the presence of so many oestrogenic chemicals in the breast must influence resulting oestrogenic responses, and the impact of this additional oestrogenic burden needs to be taken into account in future studies on growth regulation of human breast cancer cells.

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