Phytoestrogens on the Proliferation of Breast Cancer Cell MCF-7

2021 ◽  
Vol 7 (5) ◽  
pp. 3276-3285
Author(s):  
Shuyan Cai ◽  
Huimin Song ◽  
Haoliang Wu ◽  
Gang Gao ◽  
Jianwei Zheng
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Calf Serum ◽  
Proliferation Index ◽  
Control Group ◽  
Biological Macromolecules ◽  
Bovine Embryo ◽  
Solvent Control ◽  
Mcf 7

A cell is an organic whole containing biological macromolecules such as nucleic acid and protein. Human cells contain about 15,000 proteins, which play an important role in the development of cell life. This article aims to study the effect of phytoestrogens on the proliferation of breast cancer cells MCF-7. The estrogen-dependent MCF-7 cells described in this article are grown on average DMEM (containing calf serum 10) and connected to single cell culture. Five days before adding the test product, the cells were washed with PBS and converted into red-free phenol. High-sugar DMEM containing 5 parts of bovine embryo serum was cultured and treated with activated charcoal glucan glycosides. In the experiment, four dose groups of solvent control, estrogen control, anti-estrogens and two test substances were used for control, and the proliferation of MCF-7 cells was analyzed by integration method and flow cytometry. The experimental results in this article show that compared with the solvent control group, GS can significantly inhibit MCF-7 cell proliferation and cell DNA synthesis, and G/M can block the cell cycle and produce a similar inhibitory effect. 96mol/L zein treatment for 24 hours can significantly promote MCF-7 cell proliferation and cell DNA composition, promote cell cycle, and increase cell separation and proliferation index.

Phytoestrogens on the Proliferation of Breast Cancer Cell MCF - 7

2021 ◽  
Vol 7 (4) ◽  
pp. 422-431
Author(s):  
Shuyan Cai ◽  
Huimin Song ◽  
Haoliang Wu ◽  
Gang Zhi Gao ◽  
Jianwei Zheng
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Calf Serum ◽  
Proliferation Index ◽  
Control Group ◽  
Biological Macromolecules ◽  
Bovine Embryo ◽  
Solvent Control ◽  
Mcf 7

A cell is an organic whole containing biological macromolecules such as nucleic acid and protein. Human cells contain about 15,000 proteins, which play an important role in the development of cell life. This article aims to study the effect of phytoestrogens on the proliferation of breast cancer cells MCF - 7. The estrogen - dependent MCF - 7 cells described in this article are grown on average DMEM (containing calf serum 10) and connected to single cell culture. Five days before adding the test product, the cells were washed with PBS and converted into red - free phenol. High - sugar DMEM containing 5 parts of bovine embryo serum was cultured and treated with activated charcoal glucan glycosides. In the experiment, four dose groups of solvent control, estrogen control, anti - estrogens and two test substances were used for control, and the proliferation of MCF - 7 cells was analyzed by integration method and flow cytometry. The experimental results in this article show that compared with the solvent control group, GS can significantly inhibit MCF - 7 cell proliferation and cell DNA synthesis, and G/M can block the cell cycle and produce a similar inhibitory effect. 96mol/L zein treatment for 24 hours can significantly promote MCF - 7 cell proliferation and cell DNA composition, promote cell cycle, and increase cell separation and proliferation index.

Functional and molecular identification of intermediate-conductance Ca2+-activated K+ channels in breast cancer cells: association with cell cycle progression

2004 ◽  
Vol 287 (1) ◽  
pp. C125-C134 ◽  
Author(s):  
Halima Ouadid-Ahidouch ◽  
Morad Roudbaraki ◽  
Philippe Delcourt ◽  
Ahmed Ahidouch ◽  
Nathalie Joury ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Membrane Potential ◽  
Current Density ◽  
Cell Cycle Progression ◽  
G1 Phase ◽  
Cycle Progression ◽  
Mcf 7 ◽  
In Cells

We have previously reported that the hEAG K+ channels are responsible for the potential membrane hyperpolarization that induces human breast cancer cell progression into the G1 phase of the cell cycle. In the present study, we evaluate the role and functional expression of the intermediate-conductance Ca2+-activated K+ channel, hIK1-like, in controlling cell cycle progression. Our results demonstrate that hIK1 current density increased in cells synchronized at the end of the G1 or S phase compared with those in the early G1 phase. This increased current density paralleled the enhancement in hIK1 mRNA levels and the highly negative membrane potential. Furthermore, in cells synchronized at the end of G1 or S phases, basal cytosolic Ca2+ concentration ([Ca2+]i) was also higher than in cells arrested in early G1. Blocking hIK1 channels with a specific blocker, clotrimazole, induced both membrane potential depolarization and a decrease in the [Ca2+]i in cells arrested at the end of G1 and S phases but not in cells arrested early in the G1 phase. Blocking hIK1 with clotrimazole also induced cell proliferation inhibition but to a lesser degree than blocking hEAG with astemizole. The two drugs were essentially additive, inhibiting MCF-7 cell proliferation by 82% and arresting >90% of cells in the G1 phase. Thus, although the progression of MCF-7 cells through the early G1 phase is dependent on the activation of hEAG K+ channels, when it comes to G1 and checkpoint G1/S transition, the membrane potential appears to be primarily dependent on the hIK1-activity level.

scholarly journals Metformin suppresses the proliferation and invasion through NF-kB and MMPs in MCF-7 cell line

2019 ◽  
Vol 45 (3) ◽  
pp. 295-304
Author(s):  
Nail Besli ◽  
Guven Yenmis ◽  
Matem Tunçdemir ◽  
Elif Yaprak Sarac ◽  
Sibel Doğan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Line ◽  
Cancer Cell Line ◽  
Immunocytochemical Staining ◽  
Breast Adenocarcinoma ◽  
Control Group ◽  
Expression Levels ◽  
Er Positive ◽  
Mcf 7

AbstractObjectiveMCF-7 cells, a breast cancer cell line, are used for experiments of estrogen receptor (ER)-positive breast cancer and many sub-clones representing different classes of ER-positive tumors. We aimed to determine the efficacy of metformin, a potential anti-cancer agent, on the cell proliferation, and the expressions of NF-kB (p65), MMP-2 and MMP-9 in MCF-7 cell line.Materials and methodsMCF-7 cells (human breast adenocarcinoma) were treated with elevating doses of metformin (0–50 mM) for 24 h. The anti-proliferative effect of metformin was studied by BrdU proliferation assay, and the expression levels of NF-kB (p65), MMP-2 and MMP-9 were analyzed by immunocytochemical staining.ResultsThe percentage of cell proliferation was reduced significantly by 10 and 50 mM doses of metformin (p < 0.001). The expression levels of nuclear NF-kB (p65), MMP-9 and MMP-2 were considerably reduced in 50 mM metformin treated cells while the expression of cytoplasmic NF-kB (p65) elevated compared to control group (p < 0.05). Ten millimolar metformin also reduced expression of MMP-9 significantly (p < 0.05).ConclusionMetformin may act on the proliferation, and the processes of invasion and metastasis of MCF-7 cells through blocking NF-kB, which is intensely expressed in breast cancer cells, and through diminishing the expression of MMP-2 and MMP-9 significantly.

scholarly journals Ginsenoside induces cell death in breast cancer cells via ROS/PI3K/Akt signaling pathway

2020 ◽  
Vol 19 (8) ◽  
pp. 1631-1636
Author(s):  
Lihong He ◽  
Xiaorui Wang ◽  
Qing Ma ◽  
Weipeng Zhao ◽  
Yongsheng Jia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Mechanism Of Action ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Protein Expressions ◽  
Mcf 7

Purpose: To study the influence of ginsenoside on breast carcinoma, and the mechanism of action involved.Methods: Different concentrations of ginsenoside were used to treat MCF-7 breast cancer cell line. Cell viability was measured by MTT assay, while protein expressions of p-Akt and p-PI3K were determined using Western blotting. The concentrations of reactive oxidative reactants and reactive oxygen species (ROS) were assessed using fluorescence immunoassay and immunofluorescence assay. The mechanism of action involved in ginsenoside-mediated apoptosis was determined based on ROS/PI3K/Akt signaling pathway.Results: There was no change in the inhibition of MCF-7 cell proliferation in control cells with time (p > 0.05). However, inhibition of MCF-7 cell proliferation in ginsenoside group was significantly higher than that in the control group (p < 0.05); furthermore, it increased with time and ginsenoside concentration. Apoptosis was markedly and concentration-dependently higher in ginsenoside-treated MCF-7 cells than in controls (p > 0.05). There were lower protein levels of p-PI3K and p-Akt in ginsenoside-exposed MCF-7 cells than in control group; the protein expressions  decreased with increase in ginsenoside concentration (p < 0.05). The expressions of ROS in ginsenoside-treated MCF-7 cells declined, relative to the untreated group; in addition, the expressions decreased with increase in ginsenoside concentration (p < 0.05).Conclusion: Ginsenoside suppresses proliferation of MCF-7 cell line, and exerts apoptotic effect on the cells via inhibition of the ROS/PI3K/Akt signal pathway. This provides a new approach to treat breast cancer. Keywords: Breast cancer cells, Ginsenoside, Apoptosis, ROS/PI3K/Akt signaling pathway

scholarly journals GLUTATHIONE AND GLUTAREDOXIN IN ROSCOVITINE-MEDIATED INHIBITION OF BREAST CANCER CELL PROLIFERATION

2017 ◽  
Vol 72 (4) ◽  
pp. 261-267 ◽  
Author(s):  
E. V. Shakhristova ◽  
E. A. Stepovaya ◽  
O. L. Nosareva ◽  
E. V. Rudikov ◽  
V. V. Novitsky
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Protein Kinase ◽  
Breast Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Breast Cancer Cell Proliferation ◽  
Dependent Protein Kinase ◽  
Dependent Protein ◽  
Mcf 7

Background: Breast tumors are number one cause of cancer morbidity and mortality among women around the world, and Russia is not an exception. Many proteins that control proliferation of immortalized cells are redox-regulated, which is essential for modulating cellular proliferative activity, especially during tumor growth. Studying the role of glutaredoxin and glutathione in cell cycle phase distribution will allow not only to identify the molecular targets regulating cell proliferation, but also to develop methods of diagnosis and targeted therapy of socially sensitive diseases, including breast cancer, in the future.Aims: To evaluate the role of glutathione and glutaredoxin in the molecular mechanisms regulating MCF-7 breast cancer cell proliferation under the effects of roscovitine, a cyclin-dependent protein kinase inhibitor.Materials and methods: The MCF-7 cell line (human breast adenocarcinoma) was used in the study. The cell culture was incubated in the presence and absence of roscovitine in the final concentration of 20 µmol for 18 h. The production of reactive oxygen species, the distribution of cells between cell cycle phases and the amount of Annexin V positive cells were determined using flow cytometry. The concentrations of total, reduced and oxidized glutathione, protein SH groups and protein-bound glutathione were measured by spectrophotometry. The levels of glutaredoxin, cyclin E and cyclin-dependent protein kinases were estimated by Western blotting with monoclonal antibodies.Results: The effects of roscovitine in the MCF-7 cells resulted in cell cycle arrest in G2/М phases with the decreased levels of cyclin E and cyclin-dependent protein kinase 2. It was accompanied by activation of programmed cell death. In tumor cells incubated in the presence of roscovitine, oxidative stress was triggered, which was accompanied by the elevated generation of reactive oxygen species, the decrease in the concentration of reduced glutathione, and the rise in the level of glutaredoxin. It contributed to the increase in protein glutathionylation against the backdrop of the decreased SH group concentration.Conclusions: Breast cancer cell proliferation under the effects of roscovitine is reduced following not only the decrease in the cyclin level and cyclin-dependent protein kinase activity, but also the shift in the intracellular oxidant/antioxidant ratio. Roscovitine-induced oxidative stress in the MCF-7 cells contributed to protein glutathionylation with the changes in the protein structure and functions. It results in impaired cell cycle progression, indicating a possibility to regulate cellular proliferation through modulating functional properties of redox-dependent proteins using the glutathione/glutaredoxin system.

The Effect of Nano Albumin Combined with Paclitaxel on Drug Resistance of Breast Cancer Through Regulating ATP Binding Cassette Subfamily B Member 1 (ABCB1)

2022 ◽  
Vol 12 (5) ◽  
pp. 964-970
Author(s):  
Tao Liu ◽  
Xiang Wen ◽  
Qi-Jun Zhao ◽  
Ying Bai ◽  
Qing-Gang Tian
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Drug Resistance ◽  
Tumor Growth ◽  
Cell Group ◽  
High Concentration ◽  
Inhibiting Effect ◽  
S Period ◽  
Mcf 7

The paclitaxel is a common-used chemotherapy drug and its combination with nano albumin reduces drug side effect. However, whether nab-paclitaxel affects drug resistance of breast cancer remains unclear. This study intends to discuss the mechanism of drug resistance induced by nab-paclitaxel. The drug resistance of MCF-7/nab-paclitaxel in MCF-7 cell and cell proliferation was detected by MTT along with analysis of ABCB1 expression, cell cycle, and apoptosis. There was stronger drug resistance of nab-paclitaxel in the MCF-7/nab-paclitaxel cell group through be adopted with different concentration of nab-paclitaxel at the 0th hour, 24th hour and 48th hour. There was remarkable abnormal expression of the ABCB1 in the MCF-7/nab-paclitaxel cell group. The si-ABCB1 could release the quantity of the MCF-7/nab-paclitaxel cell blocked at S period. And the si-ABCB1 could reduce the expression of cyclin D1 and CDK2 in the MCF-7/nab-paclitaxel cell notably. But the expression level of p21 was increased when there was high concentration of si-ABCB1. The si-ABCB1 could increase the quantity of the MCF-7/nab-paclitaxel cell at the later period of cell apoptosis notably. The rat’s tumor growth was delayed obviously at the MCF-7/nabpaclitaxel cell group treated by si-ABCB1. But the inhibiting effect of the MCF-7/nab-paclitaxel cell on tumor growth was less. There was stronger drug resistance of cell for the nano albumin combined with paclitaxel. The function of cell proliferation in breast cancer was restrained by the nano albumin combined with paclitaxel mainly through inducing the expression of ABCB1, adjusting the growth of cell cycle and the expression of P21/BCL-2 protein.

scholarly journals Temporal and spatial topography of cell proliferation in cancer.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 3122-3122
Author(s):  
Sheheryar Kairas Kabraji ◽  
Giorgio Gaglia ◽  
Danae Argyropoulou ◽  
Yang Dai ◽  
Shu Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Spatial Organization ◽  
Disease Free Survival ◽  
Proliferation Index ◽  
Clinical Samples ◽  
Cell Cycle Protein

3122 Background: Tumors are complex ecosystems where exogenous and endogenous cues are integrated to either stimulate or inhibit cancer cell proliferation. However, the nature of these complex cell cycle states, their spatial organization, response to perturbation, and implications for clinical outcomes, are poorly characterized in tumor tissues. Methods: We used multiplexed tissue imaging to develop a robust classifier of proliferation, the multivariate proliferation index (MPI), using 513 unique tumors across five cancer types. Next, we used dimensionality reduction analysis to assess how the patterns of cell cycle protein expression in tumors were altered in response to perturbation. Results: The MPI outperforms single markers, like Ki67, when classifying proliferative index across diverse tumor types and reveals the proliferative architecture of tumors in situ. We find that proliferative and non-proliferative cancer cells are organized across microscopic (cell-to-cell) and macroscopic (tissue-level) scales. Both domains are reshaped by therapy, and local clusters of proliferative and non-proliferative tumor cells preferentially neighbor distinct tumor-infiltrating immune cells. We further phenotyped non-proliferating cancer cells using markers of quiescent cancer cells, cancer stem cells, and dormant cancer cells. We found that these types of non-proliferating cancer cells can occupy distinct regions within the same primary tumor. In high-dimensional marker space, populations of proliferative cancer cells express canonical patterns of cell cycle protein markers, a property we refer to as “cell cycle coherence”. Untreated tumors exist in a continuum of coherence states, ranging from optimal coherence, akin to freely cycling cells in culture, to reduced coherence characterized by either cell cycle polarization or non-canonical marker expression. Coherence can be stereotypically altered by induction and abrogation of mitogen signaling in a HER2-driven model of breast cancer. Cell cycle coherence is modulated by neoadjuvant therapy in patients with localized breast cancer, and coherence is associated with disease-free survival after adjuvant therapy in patients with colorectal cancer, mesothelioma and glioblastoma. Conclusions: The MPI robustly defines proliferating and non-proliferating cells in tissues, with immediate implications for clinical practice and research. The coherence metrics capture the diversity of post-treatment cell cycle states directly in clinical samples, a fundamental step in advancing precision medicine. More broadly, replacing binary metrics with multivariate traits provides a quantitative framework to study temporal processes from fixed static images and to investigate the rich spatial biology of human cancers.

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