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

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.

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SOX4 Serves an Oncogenic Role in the Tumourigenesis of Human Breast Adenocarcinoma by Promoting Cell Proliferation, Migration and Inhibiting Apoptosis

Recent Patents on Anti-Cancer Drug Discovery ◽

10.2174/1574892815666200212112119 ◽

2020 ◽

Vol 15 (1) ◽

pp. 49-58

Author(s):

Junhe Zhang ◽

Shujie Chai ◽

Xinyu Ruan

Keyword(s):

Breast Cancer ◽

Cell Proliferation ◽

Caspase 3 ◽

Breast Adenocarcinoma ◽

Migration Ability ◽

Expression Levels ◽

Apoptosis Rate ◽

And Migration ◽

Mcf 7 ◽

Proliferation And Migration

Background: Breast cancer is among the most common malignant cancers worldwide, and breast adenocarcinoma in glandular tissue cells has excessive metastasis and invasion capability. However, little is known on the molecular process by which this disease develops and progresses. Objective: In this study, we explored the effects of sex-determining region Y-box 4 (SOX4) protein on proliferation, migration, apoptosis and tumourigenesis of breast adenocarcinoma and its possible mechanisms. Methods: The SOX4 overexpression or knockdown Michigan Cancer Foundation-7 (MCF-7) cell lines were established. Among the SOX4 overexpression or MCF-7 knockdown cell lines, proliferation, migration ability and apoptosis rate were detected. The expression levels of apoptosis-related proteins (Bax and Cleaved caspase-3) were analysed using Western blot. The effect of SOX4 on tumourigenesis was analysed using the clone formation assay in vitro and tumour xenograft experiment in nude mice. Results: Compared with the overexpression of control cells, proliferation and migration ability of SOX4 overexpression cells significantly increased, the apoptosis rate significantly decreased in addition to the expression levels of Bax and Cleaved caspase-3 (P < 0.05). Compared with the knockdown of control cells, proliferation and migration ability of SOX4 knockdown cells significantly decreased, and the apoptosis rate and expression levels of Bax and Cleaved caspase-3 significantly increased (P < 0.05). Clone formation and tumour growth abilities of SOX4 overexpression cells were significantly higher than those of the control cells (P < 0.05), whereas SOX4 knockdown cells had the opposite effect. Conclusion: SOX4 plays an oncogenic role in breast adenocarcinoma tumourigenesis by promoting cell proliferation, migration and inhibiting apoptosis. It can be used as a potential molecular target for breast cancer gene therapy.

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Estradiol promotes rapid degradation of HER3 in ER-positive breast cancer cell line MCF-7

Biochemistry and Biophysics Reports ◽

10.1016/j.bbrep.2018.10.008 ◽

2018 ◽

Vol 16 ◽

pp. 103-109

Author(s):

Junko Suga ◽

Keiko Izumiyama ◽

Nobuyuki Tanaka ◽

Shigehira Saji

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

Rapid Degradation ◽

Er Positive ◽

Positive Breast Cancer Cell ◽

Mcf 7 ◽

Positive Breast Cancer

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The Effect of Micro RNA-34a and carboplatin combination on the inducing apoptosis of Breast Cancer Cell line

10.21203/rs.3.rs-289066/v1 ◽

2021 ◽

Author(s):

Sajjad Eslamkhah ◽

Nazila Alizadeh ◽

Sahar Safaei ◽

Mohammad Amini ◽

ahad Mokhtarzadeh ◽

...

Keyword(s):

Breast Cancer ◽

Cell Viability ◽

Cancer Cells ◽

Cell Line ◽

Caspase 3 ◽

Cancer Cell Line ◽

Micro Rna ◽

Control Group ◽

Expression Levels ◽

Micro Rnas

Abstract Aim: Breast cancer (BC) has been classified among the main causes of death owing to females' cancer. Carboplatin is a platinum-based chemotherapeutic drug that is an important treatment option for BC. But high and frequent doses of carboplatin usually reducing the reaction of cancer cells to medication. There is an immediate need to establish methods for increasing the carboplatin susceptibility to BC cells. For instance, micro RNAs (miRNAs) such as MiR34a demonstrate significant potential. Considering that, this research was planned to explore the better clinical effect and underlying mechanism of miR-34a as a possible tumor inhibitor and drug resistance regulator in compound with carboplatin chemotherapy drug in the cell lines of BC in humans. Methods: MCF-7 cell line was transfected with miR-34a to perform functional analyses. Subsequently, the MTT assay was applied to assess cell viability. Cell viability and cell death associated gene expression amounts including Bax, Bcl-2, caspase-3, MDR1, P53, and mir34-a, were examined through real-time quantitative PCR. Results: Findings showed that miR-34a upregulation significantly decreased MCF7 cell viability in comparison with control group. Furthermore, separate treatment of cells with miR-34a mimics and carboplatin could significantly increase Bax, Caspase-3, P53, and decrease in Bcl-2 mRNA expression levels evaluated to the non-treated group. Moreover, by reduction in expression levels of the MDR1 gene, BC cells' reaction to carboplatin has increased via miR-34a. Conclusion: In line with the findings, it could be inferred that miR-34a may improve the responsiveness of breast cancer cells to carboplatin chemotherapy with downregulation of MDR1.

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Leccinum vulpinum Watling induces DNA damage, decreases cell proliferation and induces apoptosis on the human MCF-7 breast cancer cell line

Food and Chemical Toxicology ◽

10.1016/j.fct.2016.02.005 ◽

2016 ◽

Vol 90 ◽

pp. 45-54 ◽

Cited By ~ 16

Author(s):

Filipa S. Reis ◽

Diana Sousa ◽

Lillian Barros ◽

Anabela Martins ◽

Patricia Morales ◽

...

Keyword(s):

Breast Cancer ◽

Cell Proliferation ◽

Dna Damage ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

Mcf 7

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Mild Glucose Starvation Induces KDM2A-Mediated H3K36me2 Demethylation through AMPK To Reduce rRNA Transcription and Cell Proliferation

Molecular and Cellular Biology ◽

10.1128/mcb.00579-15 ◽

2015 ◽

Vol 35 (24) ◽

pp. 4170-4184 ◽

Cited By ~ 26

Author(s):

Yuji Tanaka ◽

Hirohisa Yano ◽

Sachiko Ogasawara ◽

Sho-ichi Yoshioka ◽

Hiromi Imamura ◽

...

Keyword(s):

Breast Cancer ◽

Cell Proliferation ◽

Cell Line ◽

Breast Cancer Cell Line ◽

Triple Negative ◽

Cancer Cell Line ◽

Glucose Starvation ◽

Rrna Transcription ◽

Cancer Tissues ◽

Mcf 7

Environmental conditions control rRNA transcription. Previously, we found that serum and glucose deprivation induces KDM2A-mediated H3K36me2 demethylation in the rRNA gene (rDNA) promoter and reduces rRNA transcription in the human breast cancer cell line MCF-7. However, the molecular mechanism and biological significance are still unclear. In the present study, we found that glucose starvation alone induced the KDM2A-dependent reduction of rRNA transcription. The treatment of cells with 2-deoxy-d-glucose, an inhibitor of glycolysis, reduced rRNA transcription and H3K36me2 in the rDNA promoter, both of which were completely dependent on KDM2A in low concentrations of 2-deoxy-d-glucose, that is, mild starvation conditions. The mild starvation induced these KDM2A activities through AMP-activated kinase (AMPK) but did not affect another AMPK effector of rRNA transcription, TIF-IA. In the triple-negative breast cancer cell line MDA-MB-231, the mild starvation also reduced rRNA transcription in a KDM2A-dependent manner. We detected KDM2A in breast cancer tissues irrespective of their estrogen receptor, progesterone receptor, and HER2 status, including triple-negative cancer tissues. In both MCF-7 and MDA-MB-231 cells, mild starvation reduced cell proliferation, and KDM2A knockdown suppressed the reduction of cell proliferation. These results suggest that under mild glucose starvation AMPK induces KDM2A-dependent reduction of rRNA transcription to control cell proliferation.

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RGD peptide-mediated liposomal curcumin targeted delivery to breast cancer cells

Journal of Biomaterials Applications ◽

10.1177/0885328220949367 ◽

2020 ◽

pp. 088532822094936

Author(s):

Reza Mahmoudi ◽

Seyedeh Ashraf Mirahmadi-Babaheidri ◽

Hamdollah Delaviz ◽

Mohamad Hassan Fouani ◽

Mohsen Alipour ◽

...

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Targeted Delivery ◽

Cytotoxic Effect ◽

Cancer Cell Line ◽

Control Group ◽

Mcf 7

In this study, turmeric's active ingredient (Curcumin) was encapsulated into RGD modified Liposomes (RGD-Lip-Cur) its cytotoxic effect on the breast cancer cell line (MCF-7) was evaluated by MTT, flow cytometry and Caspase assay. Liposomes were characterized using transmission electron microscopy (TEM). Results demonstrated that the liposomes were spherical in shape, ranging from 70 to 100 nm. MTT assay revealed that RGD-Lip-Cur had a significant cytotoxic effect on MCF-7 cells at concentrations of 32, 16 and 4 μg/ml compared to Lip-Cur (P < 0.05) and curcumin (P < 0.01). The apoptosis assay demonstrated that RGD-Lip-Cur induces the apoptosis in MCF-7 cells (39.6% vs 40.2% for initial and secondary apoptosis) significantly more than Lip-Cur (67.7% vs 9.16% for initial and secondary apoptosis) and free curcumin (7.84% vs 38.8% for initial and secondary apoptosis). Moreover, caspase assay showed that RGD-Lip-Cur activates caspase 3/7 compared to Lip-Cur (P < 0.05) and free curcumin (P < 0.01). The RGD-Lip-Cur was similar to the control group and had no significant cytotoxicity effect. It is concluded that RGD-Lip-Cur as a novel carrier have high cytotoxicity effect on breast cancer cell line (MCF-7).

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MicroRNA-21 and PTEN Expression Levels Are Negatively Correlated in Doxorubicin Resistant MCF-7 Breast Cancer Cell Line

10.20944/preprints201903.0287.v1 ◽

2019 ◽

Author(s):

Indwiani Astuti ◽

Gusti Muhammad Sofyannoor ◽

Risky Oktriani ◽

Tirta Wardana ◽

Sumadi Lukman Anwar ◽

...

Keyword(s):

Breast Cancer ◽

Cell Line ◽

Cancer Cell Line ◽

Pten Expression ◽

Resistant Variant ◽

Apoptosis Pathway ◽

Mortality And Morbidity ◽

Expression Levels ◽

Mcf 7

Background: Breast cancer is the leading cause of cancer mortality and morbidity among Indonesian women. Identification of biological pathways leading into therapeutic resistance through in vitro model is an important step to develop alternative effective therapy in breast cancer. Loss of PTEN expression has been associated with resistance to chemotherapy by involving PI3K/PTEN- dependent apoptosis pathway. We conducted in vitro experiment to investigate the association of hsa-miR-21 and PTEN expression in Doxorubicin-resistant MCF-7 cell line. Methods:  Parental MCF-7 cells were periodically incubated with Doxorubicin to obtain specific Dox-resistant variant determined by IC50 using MTT assay. PTEN protein expression was analyzed using immunocytochemistry. Expression of mature has-miR-21 was measured using qRT-PCR. Results: The IC50 of Doxorubicin in parental MCF-7 and Doxorubicin-resistant MCF-7 cells (MCF-7/Dox) was 0.68 and 5.78 µg/ml, respectively. Hsa-miR-21 was significantly overexpressed in MCF-7/Dox cells compared to parental MCF cells (7.94 fold changes). Conclusion: PTEN and hsa-miR-21 expression levels were negatively correlated in Doxorubicin resistant-MCF cells. Further study to confirm the causal relationship of miR-21 overexpression and PTEN downregulation in MCF-7/Dox is required.

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