CRE-Transcription Factor Decoy Oligonucleotide Inhibition of MCF-7 Breast Cancer Cells:  Cross-Talk with p53 Signaling Pathway

Biochemistry ◽  
2000 ◽  
Vol 39 (16) ◽  
pp. 4863-4868 ◽  
Author(s):  
Youl Nam Lee ◽  
Yun Gyu Park ◽  
Yung Hyun Choi ◽  
Yee Sook Cho ◽  
Yoon S. Cho-Chung
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
P53 Signaling ◽  
Transcription Factor Decoy ◽  
Decoy Oligonucleotide ◽  
P53 Signaling Pathway ◽  
Mcf 7

scholarly journals Exploring the Mechanism of Baicalin Intervention in Breast Cancer Based on MicroRNA Microarrays and Bioinformatics Strategies

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Anqi Ge ◽  
Lifang Liu ◽  
Xian’guang Deng ◽  
Jun Luo ◽  
Yanghua Xu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Enrichment Analysis ◽  
Dependent Manner ◽  
P53 Signaling ◽  
Microrna Microarrays ◽  
P53 Signaling Pathway ◽  
Mcf 7

Objective. To explore the mechanism of baicalin intervention in breast cancer based on microRNA microarrays. Methods. The inhibitory rate of baicalin intervention in MCF-7 breast cancer cells was determined by MTT. Then, the miRNA microarrays were used to validate the key microRNAs. After that, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to validate microRNA, hsa-miR-15a, hsa-miR-100, hsa-miR-16, and hsa-miR-7t. Finally, the potential targets of these key microRNAs are predicted by miRWalk, and DAVID was utilized for gene ontology (GO) enrichment analysis and pathway enrichment analysis. Results. Baicalin may inhibit the proliferation of MCF-7 cells in a dose-dependent and time-dependent manner. The concentration of baicalin 150 μmol/L was determined for the subsequent miRNA chip research. A total of 92 upregulated microRNAs and 35 downregulated microRNAs were obtained. The upregulated miRNAs include hsa-miR-6799-5p, hsa-miR-6126, hsa-miR-4792, hsa-miR-6848-5p, hsa-miR-3197, hsa-miR-6779-5p, and hsa-miR -654-5p. The downregulated miRNAs include hsa-miR-3911, hsa-miR-504-5p, hsa-miR-30a-3p, hsa-miR-193b-3p, and hsa-miR-181b-5p. Then, differentially expressed miRNA was verified by qRT-PCR. The results showed that the expression of hsa-miR-15a, hsa-miR-100, hsa-miR-16, and hsa-let-7c was upregulated ( P < 0.05 ), which was consistent with the results of the miRNA microarray. The enrichment analysis showed that baicalin might regulate the DNA-templated proliferation, DNA-templated transcription, p53 signaling pathway, etc., of MCF-7 breast cancer cells through miRNA. Conclusion. Baicalin inhibits the proliferation of breast cancer cells. It may achieve antitumor effects through regulating microRNAs so as to affect the DNA replication (such as cellular response to DNA damage stimulus and DNA binding), RNA transcription (such as regulation of transcription, DNA-templated, transcription from RNA polymerase II promoter, and transcription factor binding), protein synthesis (such as mRNA binding, Golgi apparatus, and protein complex), endocytosis, pathways in cancer, p53 signaling pathway, and so on.

scholarly journals Folate-targeted PTEN/AKT/P53 signaling pathway promotes apoptosis in breast cancer cells

Pteridines ◽  
2020 ◽  
Vol 31 (1) ◽  
pp. 158-164
Author(s):  
Hexian Wang ◽  
Qiang Fan ◽  
Longlong Zhang ◽  
Danli Shi ◽  
Haibo Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Folic Acid ◽  
Cell Viability ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
P53 Protein ◽  
Specific Inhibitor ◽  
P53 Signaling ◽  
P53 Signaling Pathway

AbstractObjective Folate deficiency is closely related to the occurrence of human tumors and plays an important role in cell growth, differentiation, repair, and host defense. We studied the effects of folic acid on the apoptosis of breast cancer cells (MDA-MB-231) and on the activity of the PTEN/AKT/P53 signaling pathway in breast cancer cells.Methods Breast cancer cells (MDA-MB-231) were treated with folate alone or in combination with a PTEN specific inhibitor, SF1670. Cell viability was detected by a MTT assay, and the expression levels of apoptosis-related proteins and PTEN/AKT/P53 signaling pathway were detected via Western blot analysis. Rate of apoptosis was measured via cytometry.Results Folic acid inhibited the cell viability of MDAMB-231 cells and the expressions of Bcl-2 and p-AKT proteins and upregulate the expression of Bax, PTEN, and P53 proteins, thereby inducing apoptosis in these cells. SF1670 treatment inhibited the expressions of Bcl-2 and p-AKT protein and upregulate Bax, PTEN, and P53 protein expression.Conclusion Folic acid has cytotoxic effects on MDAMB-231 cells and can induce apoptosis by targeting the PTEN/AKT/P53 signaling pathway.

scholarly journals Effects of different glucose concentrations on the leptin signaling pathway in MCF-7 and T47D breast cancer cells

2019 ◽  
Vol 26 (12) ◽  
pp. 2966
Author(s):  
Pinar Demirel ◽  
Umit Ozorhan ◽  
Bilge Tuna ◽  
Margot Cleary ◽  
Soner Dogan
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Leptin Signaling ◽  
Mcf 7

scholarly journals gef Gene Expression in MCF-7 Breast Cancer Cells is Associated with a Better Prognosis and Induction of Apoptosis by p53-Mediated Signaling Pathway

2011 ◽  
Vol 12 (11) ◽  
pp. 7445-7458 ◽  
Author(s):  
Houria Boulaiz ◽  
Pablo J. Álvarez ◽  
Jose Prados ◽  
Juan Marchal ◽  
Consolación Melguizo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Induction Of Apoptosis ◽  
Mcf 7
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