Energy metabolism targeted drugs synergize with photodynamic therapy to potentiate breast cancer cell death

2014 ◽  
Vol 13 (12) ◽  
pp. 1793-1803 ◽  
Author(s):  
Xiaolan Feng ◽  
Yi Zhang ◽  
Pan Wang ◽  
Quanhong Liu ◽  
Xiaobing Wang
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Energy Metabolism ◽  
Combination Therapy ◽  
Breast Cancer Cells ◽  
Ros Generation ◽  
Targeted Drugs ◽  
Cancer Cell Death ◽  
Dependent Cell

Glycolytic inhibitors can synergistically enhance the photosensitivity of breast cancer cells by triggering cellular mitochondria- and caspase-dependent cell apoptosis, which was induced by additional ROS generation in combination therapy.

scholarly journals Estrogen as Jekyll and Hyde: regulation of cell death

F1000Research ◽  
2014 ◽  
Vol 3 ◽  
pp. 161 ◽  
Author(s):  
Wen Zhou ◽  
Xiaoxia Zhu
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Breast Cancer Cells ◽  
Breast Cancer Patients ◽  
Physiological Level ◽  
Cancer Cell Death ◽  
Er Positive ◽  
Nfκb Pathway ◽  
Opinion Article ◽  
Positive Breast Cancer

Sustained estrogenic exposure increases the risk and/or the progression of various cancers, including those of the breast, endometrium and ovary. Unexpectedly, physiological level of estrogen together with a novel IKKα inhibitor BAY11-7082 could effectively induce cell apoptosis in ER-positive breast cancer cells, suggesting combining estrogen with IKKα inhibition may be beneficial for breast cancer patients. This opinion article touches upon the dual role estrogen played in inducing cancer cell death and asks whether use of estrogen in combination with IKKα-targeted therapy would be possible reconsider the newly identified crosstalk between ER and NFκB pathway which can be utilized to switch the effects of estrogen on cell death.

scholarly journals Hydrogen Phosphate Selectively Induces MDA-MB-231 Breast Cancer Cell Death in vitro

2021 ◽  
Author(s):  
Aya Shanti ◽  
Kenana Al Adem ◽  
Cesare Stefanini ◽  
Sungmun Lee
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Dihydrogen Phosphate ◽  
Human Breast ◽  
Hydrogen Phosphate ◽  
Cancer Cell Death ◽  
Phosphate Ions

Abstract Phosphate ions are the most abundant anions inside the cells, and they are increasingly gaining attention as key modulators of cellular function and gene expression. However, little is known about the effect of inorganic phosphate ions on cancer cells, particularly breast cancer cells. Here, we investigated the toxicity of different phosphate compounds to triple-negative human breast cancer cells (MDA-MB-231) and compared it to that of human monocytes (THP-1). We found that, unlike dihydrogen phosphate (H2PO4−), hydrogen phosphate (HPO42−) at 20 mM or lower concentrations induced breast cancer (MDA-MB-231) cell death more than immune (THP-1) cell death. We correlate this effect to the fact that phosphate in the form of HPO42− raises pH levels to alkaline levels which are not optimum for transport of phosphate into cancer cells. The results in this study highlight the importance of further exploring hydrogen phosphate (HPO42−) as a potential therapeutic for the treatment of breast cancer.

scholarly journals ROS Mediate xCT-Dependent Cell Death in Human Breast Cancer Cells under Glucose Deprivation

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1598 ◽  
Author(s):  
Mei-Chun Chen ◽  
Li-Lin Hsu ◽  
Sheng-Fan Wang ◽  
Chih-Yi Hsu ◽  
Hsin-Chen Lee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Critical Role ◽  
Glucose Deprivation ◽  
Glutathione Biosynthesis ◽  
Dependent Cell ◽  
Amp Activated Protein Kinase

xCT, also known as solute carrier family 7 member 11 (SLC7A11), the light chain of the cystine/glutamate antiporter, is positively correlated with cancer progression due to antioxidant function. During glucose deprivation, the overexpression of xCT does not protect cancer cells but instead promotes cell death. Further understanding the mechanism of glucose deprivation-induced cell death is important for developing anticancer treatments targeting the glucose metabolism. In this study, we found that breast cancer cells with a high expression of xCT demonstrated increased levels of reactive oxygen species (ROS) and were more sensitive to glucose deprivation than the cells with a low expression of xCT. However, AMP-activated protein kinase (AMPK) did not significantly affect glucose-deprivation-induced cell death. The antioxidant N-acetyl-cysteine prevented glucose-deprivation-induced cell death, and the glutathione biosynthesis inhibitor L-buthionine-S, R-sulfoximine enhanced glucose-deprivation-induced cell death. The inhibition of xCT by sulfasalazine or a knockdown of xCT reduced the glucose-deprivation-increased ROS levels and glucose-deprivation-induced cell death. Glucose deprivation reduced the intracellular glutamate, and supplementation with α-ketoglutarate prevented the glucose-deprivation-increased ROS levels and rescued cell death. The knockdown of sirtuin-3 (SIRT3) further enhanced the ROS levels, and promoted xCT-related cell death after glucose deprivation. In conclusion, our results suggested that ROS play a critical role in xCT-dependent cell death in breast cancer cells under glucose deprivation.

scholarly journals Methylene blue photodynamic therapy induces selective and massive cell death in human breast cancer cells

BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Ancély F. dos Santos ◽  
Letícia F. Terra ◽  
Rosangela A. M. Wailemann ◽  
Talita C. Oliveira ◽  
Vinícius de Morais Gomes ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Methylene Blue ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Massive Cell Death ◽  
Massive Cell

Combination therapy of Ad-mda7 and trastuzumab increases cell death in Her-2/neu–overexpressing breast cancer cells

Surgery ◽  
2004 ◽  
Vol 136 (2) ◽  
pp. 437-442 ◽  
Author(s):  
Tamra McKenzie ◽  
Yanna Liu ◽  
Michelle Fanale ◽  
Stephen G. Swisher ◽  
Sunil Chada ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Combination Therapy ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Her 2

Synergistic Enhancement of 2-Deoxy-D-Glucose-Mediated Breast Cancer Cell Death by Mitochondria-Targeted Drugs

2011 ◽  
Vol 51 ◽  
pp. S120
Author(s):  
Gang Cheng ◽  
Donna McAllister ◽  
Jacek Zielonka ◽  
Brian P. Dranka ◽  
Joy Joseph ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Targeted Drugs ◽  
Cancer Cell Death ◽  
Synergistic Enhancement

scholarly journals Induction of Redox-Mediated Cell Death in ER-Positive and ER-Negative Breast Cancer Cells by a Copper(II)-Phenolate Complex: An In Vitro and In Silico Study

Molecules ◽  
2020 ◽  
Vol 25 (19) ◽  
pp. 4504
Author(s):  
Vaiyapuri Subbarayan Periasamy ◽  
Anvarbatcha Riyasdeen ◽  
Venugopal Rajendiran ◽  
Mallayan Palaniandavar ◽  
Hanumanthappa Krishnamurthy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Late Onset ◽  
Strong Association ◽  
Ros Generation ◽  
Special Focus

This research was aimed at finding the cytotoxic potential of the mixed ligand copper(II) complex [Cu(tdp)(phen)](ClO4)—where H(tdp) is the tetradentate ligand 2-[(2-(2-hydroxyethylamino)-ethylimino)methyl]phenol, and phen is 1,10-phenanthroline—to two genotypically different breast cancer cells, MCF-7 (p53+ and ER+) and MDA-MB-231 (p53- and ER-). The complex has been already shown to be cytotoxic to ME180 cervical carcinoma cells. The special focus in this study was the induction of cell death by apoptosis and necrosis, and its link with ROS. The treatment brought about nuclear fragmentation, phosphatidylserine externalization, disruption of mitochondrial trans-membrane potential, DNA damage, cell cycle arrest at sub-G1 phase, and increase of ROS generation, followed by apoptotic death of cells during early hours and a late onset of necrosis in the cells surviving the apoptosis. The efficacy of the complex against genotypically different breast cancer cells is attributed to a strong association through p53-mitochondrial redox—cell cycle junction. The ADMET properties and docking of the complex at the active site of Top1 are desirable attributes of a lead molecule for development into a therapeutic. Thus, it is shown that the copper(II)–phenolate complex[Cu(tdp)(phen)]+ offers potential to be developed into a therapeutic for breast cancers in general and ER-negative ones in particular.

scholarly journals SRT1720 Induces Lysosomal-Dependent Cell Death of Breast Cancer Cells

2014 ◽  
Vol 14 (1) ◽  
pp. 183-192 ◽  
Author(s):  
Tyler J. Lahusen ◽  
Chu-Xia Deng
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Dependent Cell
Sign in / Sign up

Export Citation Format

Share Document