scholarly journals Antitumor Activity of Chinese Propolis in Human Breast Cancer MCF-7 and MDA-MB-231 Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Hongzhuan Xuan ◽  
Zhen Li ◽  
Haiyue Yan ◽  
Qing Sang ◽  
Kai Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Human Breast Cancer ◽  
Mitochondrial Membrane ◽  
Biological Activities ◽  
Human Breast ◽  
Antitumor Effects ◽  
Chinese Propolis ◽  
Mcf 7

Chinese propolis has been reported to possess various biological activities such as antitumor. In present study, anticancer activity of ethanol extract of Chinese propolis (EECP) at 25, 50, 100, and 200 μg/mL was explored by testing the cytotoxicity in MCF-7 (human breast cancer ER(+)) and MDA-MB-231 (human breast cancer ER(−)) cells. EECP revealed a dose- and time-dependent cytotoxic effect. Furthermore, annexin A7 (ANXA7), p53, nuclear factor-κB p65 (NF-κB p65), reactive oxygen species (ROS) levels, and mitochondrial membrane potential were investigated. Our data indicated that treatment of EECP for 24 and 48 h induced both cells apoptosis obviously. Exposure to EECP significantly increased ANXA7 expression and ROS level, and NF-κB p65 level and mitochondrial membrane potential were depressed by EECP dramatically. The effects of EECP on p53 level were different in MCF-7 and MDA-MB-231 cells, which indicated that EECP exerted its antitumor effects in MCF-7 and MDA-MB-231 cells by inducing apoptosis, regulating the levels of ANXA7, p53, and NF-κB p65, upregulating intracellular ROS, and decreasing mitochondrial membrane potential. Interestingly, EECP had little or small cytotoxicity on normal human umbilical vein endothelial cells (HUVECs). These results suggest that EECP is a potential alternative agent on breast cancer treatment.

Antitumor effects of seleno-β-lactoglobulin on human breast cancer MCF-7 and MDA-MB-231 cells in vitro

2019 ◽  
Vol 61 ◽  
pp. 104607 ◽  
Author(s):  
Xiaomeng Xu ◽  
Yingying Feng ◽  
Xiaoyu Chen ◽  
Qinjian Wang ◽  
Ting Meng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Antitumor Effects ◽  
Β Lactoglobulin ◽  
Mcf 7

Different antitumor effects of quercetin, quercetin-3′-sulfate and quercetin-3-glucuronide in human breast cancer MCF-7 cells

2018 ◽  
Vol 9 (3) ◽  
pp. 1736-1746 ◽  
Author(s):  
Qiu Wu ◽  
Paul W. Needs ◽  
Yalong Lu ◽  
Paul A. Kroon ◽  
Daoyuan Ren ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Molecular Mechanism ◽  
Human Breast Cancer ◽  
Water Soluble ◽  
Human Breast ◽  
Inhibitory Effects ◽  
Antitumor Effects ◽  
Mcf 7

This study was designed to investigate the tumor-inhibitory effects of quercetin (Que) and its water-soluble metabolites, quercetin-3′-sulfate (Q3′S) and quercetin-3-glucuronide (Q3G), as well as to make the molecular mechanism and structure-antitumor relationship clear.

Targeting Cell Necroptosis and Apoptosis Induced by Shikonin via Receptor Interacting Protein Kinases in Estrogen Receptor Positive Breast Cancer Cell Line, MCF-7

2018 ◽  
Vol 18 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Zahra Shahsavari ◽  
Fatemeh Karami-Tehrani ◽  
Siamak Salami
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Death ◽  
Membrane Potential ◽  
Cell Line ◽  
Mitochondrial Membrane Potential ◽  
Breast Cancer Cell Line ◽  
Mitochondrial Membrane ◽  
Cancer Cell Line ◽  
Mcf 7

Background: Recognition of a new therapeutic agent may activate an alternative programmed cell death for the treatment of breast cancer. Objective: Here, it has been tried to evaluate the effects of Shikonin, a naphthoquinone derivative of Lithospermum erythrorhizon, on the induction of necroptosis and apoptosis mediated by RIPK1-RIPK3 in the ER+ breast cancer cell line, MCF-7. Methods: In the current study, cell death modalities, cell cycle patterns, RIPK1 and RIPK3 expressions, caspase-3 and caspase-8 activities, reactive oxygen species and mitochondrial membrane potential have been evaluated in the Shikonin-treated MCF-7 cells. Results: Necroptosis and apoptosis have been occurred by Shikonin, with a significant increase in RIPK1 and RIPK3 expressions, although necroptosis was the major rout in MCF-7 cells. Shikonin significantly increased the percentage of the cells in sub-G1 and also those in the later stages of cell cycle, which represents an increase in necroptosis and apoptosis. Under caspase inhibition by Z-VAD-FMK, Shikonin has stimulated necroptosis, which could be arrested by Nec-1. An increase in ROS levels and a decrease in the mitochondrial membrane potential have also been observed. Conclusion: On the basis of present findings, Shikonin has been suggested as a good candidate for the induction of cell death in ER+ breast cancer, although further investigations, experimental and clinical, are required.

Trabectedin to induce mitochondrial membrane potential dissipation and reactive oxygen species generation in breast cancer cells.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e13580-e13580
Author(s):  
Harika Atmaca ◽  
Emir Bozkurt ◽  
Burcu Cakar ◽  
Zeki Gokhan Surmeli ◽  
Selim Uzunoglu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Reactive Oxygen Species ◽  
Membrane Potential ◽  
Cancer Cells ◽  
Dna Fragmentation ◽  
Human Breast Cancer ◽  
Mitochondrial Membrane ◽  
Breast Cancer Cells ◽  
Oxygen Species ◽  
Human Breast

e13580 Background: Trabectedin (Yondelis; ET-743) is a tetrahydroisoquinoline alkaloid that was originally derived from the marine tunicate Ecteinascidia turbinata and is currently prepared synthetically. It ıs currently used for the treatment of soft tissue sarcomas. It has been shown that Trabectedin provides the production of superoxides near the DNA strand, resulting in DNA backbone cleavage and cell apoptosis, however the apoptotic mechanisms of Trabectedin is still very limited. The objective of this study is to investigate the underlying mechanisms of apoptosis Trabectedin in two human breast cancer cell lines (MDA-MB-231 and MDA-MB-453) and one human immortalized non-transformed breast epithelial cell line (MCF-10A), to see if similar oxidation processes take place in breast cancer. Methods: Cytotoxicity was assessed by XTT cell viability assay. Apoptosis was shown by measuring DNA fragmentation, caspase 3/7 activation. Mitochondrial membrane potential (MMP) was evaluated by TMRE dye. Measurement of reactive oxygen species (ROS) was done by using Glutathione S-Transferase (GST) Assay Kit and CM-H2DCFDA dye. Results: Trabectedin induced the cytotoxicity in breast cancer cells in a time and dose dependent manner. Moreover, it increased DNA fragmentation and the MMP dissipation in tested breast cancer cells. The levels of ROS production in parallel with GST enzyme activity were sharply increased by Trabectedin treatment. Conclusions: This is the first study to investigate the role of Trabectedin activity and mechanisms of apoptosis in human breast cancer cells. These preliminary results might show us a way to use Trabectedin alone, or in combination for breast cancer treatment in near future.

scholarly journals Downregulation of KDR expression induces apoptosis in breast cancer cells

2014 ◽  
Vol 19 (4) ◽  
Author(s):  
Xiao Zhang ◽  
Yin-Lin Ge ◽  
Shu-Ping Zhang ◽  
Ping Yan ◽  
Run-Hua Tian
Keyword(s):  
Breast Cancer ◽  
Cytochrome C ◽  
Membrane Permeability ◽  
Human Breast Cancer ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Human Breast ◽  
Cytochrome C Release ◽  
Mitochondrial Membrane Permeability ◽  
Mcf 7

AbstractAngiogenesis plays a crucial role in the growth, invasion and metastasis of breast cancer. Vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are the key regulators of tumor angiogenesis. VEGFR-2, known as the kinase insert domain receptor (KDR), is a key receptor involved in malignant angiogenesis. We previously showed that knocking down KDR with short interference RNA (KDR-siRNA) markedly decreased KDR expression and suppressed tumor growth in a xenograft model. However, the mechanisms underlying the anti-cancer effects of KDR-siRNA are not clearly understood. This study aimed to elucidate the molecular mechanisms that induce apoptosis in human breast cancer MCF-7 cells after transfection with KDR-siRNA. We studied the effects of KDR-siRNA on proliferation, apoptosis, antiapoptotic and pro-apoptotic proteins, mitochondrial membrane permeability, cytochrome c release and caspase-3 activity. The results indicated that KDR-siRNA treatment significantly inhibited the proliferation and induced the apoptosis of MCF-7 cells, reduced the levels of the anti-apoptotic proteins, Bcl-2 and Bcl-xl, and increased the level of the pro-apoptotic protein Bax, resulting in a decreased Bcl-2/Bax ratio. KDR-siRNA also enhanced the mitochondrial membrane permeability, induced cytochrome c release from the mitochondria, upregulated apoptotic protease-activating factor-1 (Apaf-1), cleaved caspase-3, and increased caspase-3 activity in MCF-7 cells. Furthermore, KDR-siRNA-induced apoptosis in MCF-7 cells was blocked by the caspase inhibitor Z-VAD-FMK, suggesting a role of caspase activation in the induction of apoptosis. These results indicate that the Bcl-2 family proteins and caspase-related mitochondrial pathways are primarily involved in KDR-siRNAinduced apoptosis in MCF-7 cells and that KDR might be a potential therapeutic target for human breast cancer treatments.

scholarly journals Correction: Different antitumor effects of quercetin, quercetin-3′-sulfate and quercetin-3-glucuronide in human breast cancer MCF-7 cells

2019 ◽  
Vol 10 (7) ◽  
pp. 4452-4453
Author(s):  
Qiu Wu ◽  
Paul W. Needs ◽  
Yalong Lu ◽  
Paul A. Kroon ◽  
Daoyuan Ren ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Human Breast ◽  
Antitumor Effects ◽  
Mcf 7

Correction for ‘Different antitumor effects of quercetin, quercetin-3′-sulfate and quercetin-3-glucuronide in human breast cancer MCF-7 cells’ by Qiu Wu et al., Food Funct., 2018, 9, 1736–1746.

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