scholarly journals Low-Frequency Magnetic Fields (LF-MFs) Inhibit Proliferation by Triggering Apoptosis and Altering Cell Cycle Distribution in Breast Cancer Cells

2020 ◽  
Vol 21 (8) ◽  
pp. 2952
Author(s):  
Aoshu Xu ◽  
Qian Wang ◽  
Tingting Lin
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Magnetic Fields ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Glycogen Synthase ◽  
Low Frequency ◽  
Cell Cycle Distribution ◽  
Cell Proliferation Inhibition

Breast cancer is a common malignancy threatening women’s health around the world. Despite improved treatments for different subtypes of breast tumors that have been put forward, there still exists a poor therapeutic response and prognosis. Magnetic fields, as a non-invasive therapy, have shown anti-tumor effects in vitro and in vivo; however, the detailed mechanisms involved are still not clear. In this study, we found that in exposure to low-frequency magnetic fields (LF-MFs) with an intensity of 1 mT and frequencies of 50, 125, 200, and 275 Hz, separately, the proliferation of breast cancer cells was inhibited and LF-MF with 200 Hz reached the optimum inhibition effect, on exposure time-dependently. Notably, we found that exposure to LF-MF led to MCF-7 and ZR-75-1 cell apoptosis and cell cycle arrest. Moreover, we also discovered that LF-MF effectively increased the level of reactive oxygen species (ROS), suppressed the PI3K/AKT signaling pathway, and activated glycogen synthase kinase-3β (GSK-3β). We demonstrated that the GSK3β activity contributed to LF-MF-induced cell proliferation inhibition and apoptosis, while the underlying mechanism was associated with the inhibition of PI3K/AKT through increasing the intracellular ROS accumulation. These results indicate that LF-MF with a specific frequency may be an attractive therapy to treat breast cancers.

Novel Platinum(II) Complexes Selectively Induced Apoptosis and Cell Cycle Arrest of Breast Cancer Cells In Vitro

2019 ◽  
Vol 4 (44) ◽  
pp. 12971-12977
Author(s):  
Nenad Marković ◽  
Milan Zarić ◽  
Marija D. Živković ◽  
Snežana Rajković ◽  
Ivan Jovanović ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cycle Arrest ◽  
Induced Apoptosis

scholarly journals Correction: Prosopis juliflora (Sw.), DC induces apoptosis and cell cycle arrest in triple negative breast cancer cells: in vitro and in vivo investigations

Oncotarget ◽  
2018 ◽  
Vol 9 (68) ◽  
pp. 33050-33050 ◽  
Author(s):  
Bhimashankar Gurushidhappa Utage ◽  
Milind Shivajirao Patole ◽  
Punam Vasudeo Nagvenkar ◽  
Sonali Shankar Kamble ◽  
Rajesh Nivarti Gacche
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Prosopis Juliflora ◽  
Cycle Arrest

scholarly journals Prosopis juliflora (Sw.), DC induces apoptosis and cell cycle arrest in triple negative breast cancer cells: in vitro and in vivo investigations

Oncotarget ◽  
2018 ◽  
Vol 9 (54) ◽  
pp. 30304-30323 ◽  
Author(s):  
Bhimashankar Gurushidhappa Utage ◽  
Milind Shivajirao Patole ◽  
Punam Vasudeo Nagvenkar ◽  
Sonali Shankar Kamble ◽  
Rajesh Nivarti Gacche
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Prosopis Juliflora ◽  
Cycle Arrest

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 Cepharanthine Induces Autophagy, Apoptosis and Cell Cycle Arrest in Breast Cancer Cells

2017 ◽  
Vol 41 (4) ◽  
pp. 1633-1648 ◽  
Author(s):  
Sumei Gao ◽  
Xiaoyan Li ◽  
Xia Ding ◽  
Wenwen Qi ◽  
Qifeng Yang
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Invasion And Migration ◽  
Cycle Arrest ◽  
And Migration ◽  
Anti Tumour Effect

Background: Cepharanthine (CEP) is a biscoclaurine alkaloid extracted from Stephania cepharantha and has been shown to have an anti-tumour effect on different types of cancers. However, the anti-cancer effect of CEP on human breast cancer cells is still unclear. Methods: We used MTT, clone formation, in vitro scratch, invasion and migration assays to confirm the inhibitory role of CEP on the proliferation of breast cancer cells. Flow cytometry, plasmid construction and western blot analysis were used to study the detailed mechanisms. Results: Our study showed that CEP could inhibit cell proliferation by inducing autophagy, apoptosis, and G0/G1 cell cycle arrest of breast cancer cells. Furthermore, we found that CEP induced autophagy and apoptosis by inhibiting the AKT/mTOR signalling pathway. Conclusion: We found that CEP could inhibit growth and motility of MCF-7 and MDA-MB-231 breast cancer cell. Our study revealed an anti-tumour effect of CEP on breast cancer cells and suggests that CEP could be a potential new clinical therapy for breast cancer.

scholarly journals Adipocytes Under Obese-Like Conditions Change Cell Cycle Distribution and Phosphorylation Profiles of Breast Cancer Cells: The Adipokine Receptor CAP1 Matters

2021 ◽  
Vol 11 ◽  
Author(s):  
Malin Bergqvist ◽  
Karin Elebro ◽  
Signe Borgquist ◽  
Ann H. Rosendahl
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Cell Cycle Distribution ◽  
Antibody Array ◽  
Er Positive ◽  
Metabolic Conditions

BackgroundObesity and associated metabolic conditions impact adipocyte functionality with potential consequences for breast cancer risk and prognosis, but contributing mechanisms remain to be understood. The adipokine receptor adenylyl cyclase-associated protein-1 (CAP1) has been implicated in the progression of breast cancer, but results are conflicting and the underlying molecular mechanisms are still unknown. In this study, molecular and cellular effects in breast cancer cells by stimulation of adipocytes under normal or obese-like conditions, and potential involvement of CAP1, were assessed.Material and MethodsEstrogen receptor (ER)-positive T47D and ER-negative MDA-MB-231 breast cancer cells were exposed to adipocyte-secretome from adipocytes placed under pressures mimicking normal and obese-like metabolic conditions. Changes in phosphorylated kinase proteins and related biological pathways were assessed by phospho-antibody array and PANTHER analysis, cell proliferation were investigated through sulforhodamine B, cell cycle distribution by flow cytometry. Functional effects of CAP1 were subsequently examined following small interfering (si)RNA-mediated knockdown.ResultsProtein phosphorylations involved in important biological processes were enriched in T47D breast cancer cells in response to adipocyte secretome from obese-like compared with normal conditions. The obesity-associated adipocyte secretome further stimulated cell proliferation and a shift from cell cycle G1-phase to S- and G2/M-phase was observed. Silencing of CAP1 decreased cell proliferation in both T47D and MDA-MB-231 cells, and reduced the obesity-associated secretome-induction of phosphoproteins involved in cell proliferation pathways.ConclusionsThese results indicate that the adipocyte secretome and CAP1 are mechanistically important for the proliferation of both ER-positive and ER-negative breast cancer cells, and potential signaling mediators were identified. These studies provide biological insight into how obesity-associated factors could affect breast cancer.

Effect of extremely low frequency magnetic fields on the metastatic characteristics of breast cancer cells

2018 ◽  
Vol 92 ◽  
pp. S103
Author(s):  
R. Rashidnezhad ◽  
A. Madjid Ansari ◽  
M. Shokrollahy ◽  
H. Sanati ◽  
Z.S. Mesbah Moosavi
Keyword(s):  
Breast Cancer ◽  
Magnetic Fields ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Low Frequency ◽  
Extremely Low Frequency

scholarly journals Distinct Modulatory Effects of Fever-Range Hyperthermia on the Response of Breast Cancer Cells and Macrophages to Mistletoe (Viscum album L.) Extract

2021 ◽  
Vol 14 (6) ◽  
pp. 551
Author(s):  
Henryk M. Kozłowski ◽  
Małgorzata Pawlikowska ◽  
Justyna Sobocińska ◽  
Tomasz Jędrzejewski ◽  
Artur Dzialuk ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Inflammatory Factors ◽  
Cell Cycle Distribution ◽  
Distribution Analysis ◽  
Treated Breast ◽  
Treated Breast Cancer

Heat utility as a critical component of fever is often ignored, although the symptom is observed in many medical conditions. Mistletoe extract (ME) is an adjunctive medication prescribed to cancer patients. The increase in body temperature is frequently observed in patients following ME administration. Nevertheless, the impact of this fever on the effectiveness of therapy is unknown. Therefore, we aimed to investigate the effect of fever-range temperatures on ME-treated breast cancer cells and macrophages. The cells were simultaneously stimulated with ME and subjected to fever-range hyperthermia (FRH; 39 °C or 41 °C). After co-treatment, the cell viability, generation of reactive oxygen species (ROS), cell cycle distribution, and production of pro-inflammatory factors (interleukin (IL)-1β, IL-6, and cyclooxygenase (COX)-2) were evaluated. The results showed that the exposure of ME-treated breast cancer cells to FRH at 39 °C resulted in a slight decrease in their viability, whereas FRH of 41 °C enhanced this effect. Only FRH of 41 °C induced minor changes in ROS level in ME-treated breast cancer cell lines. In ME-treated macrophages, FRH stimulated cell proliferation. The cell cycle distribution analysis showed a difference between cells cultured at 39 °C and 41 °C in all examined cell lines. Moreover, hyperthermia at 41 °C completely inhibited the ME-induced increase in IL-1β and IL-6 expression in MCF-7 breast cancer cells, whereas this effect was not observed in 4T1 breast cancer cells. In contrast, in ME-treated macrophages, FRH of 41 °C strongly up-regulated expression of the pro-inflammatory factors. We conclude that fever is an important component of ME therapy that differentially affects cancer and immune cells.

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