scholarly journals Effects of caffeic acid, chlorogenic acid, and EGCG on the methylation status of p16 gene in T-47D breast cancer cells

2007 ◽  
Vol 17 (4) ◽  
pp. 522-528
Author(s):  
Won-Jun Lee
Keyword(s):  
Breast Cancer ◽  
Chlorogenic Acid ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Breast Cancer Cells ◽  
Methylation Status ◽  
P16 Gene

scholarly journals Dual Epigenetic Regulation of ERα36 Expression in Breast Cancer Cells

2019 ◽  
Vol 20 (11) ◽  
pp. 2637 ◽  
Author(s):  
Charlène Thiebaut ◽  
Amand Chesnel ◽  
Jean-Louis Merlin ◽  
Maelle Chesnel ◽  
Agnès Leroux ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mammary Epithelial Cells ◽  
Methylation Status ◽  
Acquired Resistance ◽  
Good Prognosis ◽  
Mammary Epithelial ◽  
Endogenous Expression ◽  
Epigenetic Modulation

Breast cancer remains the major cause of cancer-induced morbidity and mortality in women. Among the different molecular subtypes, luminal tumors yet considered of good prognosis often develop acquired resistance to endocrine therapy. Recently, misregulation of ERα36 was reported to play a crucial role in this process. High expression of this ERα isoform was associated to preneoplastic phenotype in mammary epithelial cells, disease progression, and enhanced resistance to therapeutic agents in breast tumors. In this study, we identified two mechanisms that could together contribute to ERα36 expression regulation. We first focused on hsa-miR-136-5p, an ERα36 3’UTR-targeting microRNA, the expression of which inversely correlated to the ERα36 one in breast cancer cells. Transfection of hsa-miR136-5p mimic in MCF-7 cells resulted in downregulation of ERα36. Moreover, the demethylating agent decitabine was able to stimulate hsa-miR-136-5p endogenous expression, thus indirectly decreasing ERα36 expression and counteracting tamoxifen-dependent stimulation. The methylation status of ERα36 promoter also directly modulated its expression level, as demonstrated after decitabine treatment of breast cancer cell and confirmed in a set of tumor samples. Taken together, these results open the way to a direct and an indirect ERα36 epigenetic modulation by decitabine as a promising clinical strategy to counteract acquired resistance to treatment and prevent relapse.

Solanum nigrum Anticancer Effect Through Epigenetic Modulations in Breast Cancer Cell Lines

2020 ◽  
Vol 16 (2) ◽  
pp. 121-126
Author(s):  
Atefeh Shirkavand ◽  
Zahra N. Boroujeni ◽  
Seyed A. Aleyasin
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Methylation Status ◽  
Cancer Cell Lines ◽  
Solanum Nigrum ◽  
Breast Cancer Cell Lines

Background: DNA methylation plays an important role in the regulation of gene expression in mammalian cells and often occurs at CpG islands in the genome. It is more reversible than genetic variations and has therefore attracted much attention for the treatment of many diseases, especially cancer. In the present study, we investigated the effect of Solanum nigrum Extract (SNE) on the methylation status of the VIM and CXCR4 genes in breast cancer cell lines. Methods: The Trypan blue assay was used to study the effect of SNE at various concentrations of 0, 0.1, 1.5, 2.5, 3.5 and 5 mg/ml for 48 h on the survival of three human breast cancer cell lines MCF7, MDA-MB-468, MDA-MB-231. Methylation status of VIM and CXCR4 genes in breast cancer cell lines was assessed by Methylation-Specific PCR (MSP) method. Also, methylation changes of VIM and CXCR4 genes in breast cancer cell lines after treatment with 0.1 mg/ml of SNE for 6 days were analyzed by MSP method. To confirm the effect of SNE on methylation of VIM and CXCR4 genes, Real-Time PCR was performed. Results: The Trypan blue assay results indicated that treatment with SNE reduced cell viability in a dose-dependent manner in breast cancer cells. Our results showed that treatment of breast cancer cells with 0.1 mg/ml of SNE hypermethylated the VIM, CXCR4 genes and significantly reduced the expression levels of their mRNA (P<0.05). Conclusion: Our findings reveal for the first time the impact of SNE on the methylation of breast cancer cells.

scholarly journals Comparison of Two Components of Propolis: Caffeic Acid (CA) and Caffeic Acid Phenethyl Ester (CAPE) Induce Apoptosis and Cell Cycle Arrest of Breast Cancer Cells MDA-MB-231

Molecules ◽  
2017 ◽  
Vol 22 (9) ◽  
pp. 1554 ◽  
Author(s):  
Agata Kabała-Dzik ◽  
Anna Rzepecka-Stojko ◽  
Robert Kubina ◽  
Żaneta Jastrzębska-Stojko ◽  
Rafał Stojko ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Breast Cancer Cells ◽  
Caffeic Acid Phenethyl Ester ◽  
Cycle Arrest

scholarly journals The Jumonji Domain-Containing Histone Demethylase Homolog 1D/lysine Demethylase 7A (JHDM1D/KDM7A) Is an Epigenetic Activator of RHOJ Transcription in Breast Cancer Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Ziyu Zhang ◽  
Baoyu Chen ◽  
Yuwen Zhu ◽  
Tianyi Zhang ◽  
Yibiao Yuan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Rna Polymerase Ii ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Methylation Status ◽  
Small Gtpase ◽  
Epigenetic Mechanism ◽  
Migration And Invasion ◽  
Breast Cancer Patients

The small GTPase RHOJ is a key regulator of breast cancer metastasis by promoting cell migration and invasion. The prometastatic stimulus TGF-β activates RHOJ transcription via megakaryocytic leukemia 1 (MKL1). The underlying epigenetic mechanism is not clear. Here, we report that MKL1 deficiency led to disrupted assembly of the RNA polymerase II preinitiation complex on the RHOJ promoter in breast cancer cells. This could be partially explained by histone H3K9/H3K27 methylation status. Further analysis confirmed that the H3K9/H3K27 dual demethylase JHDM1D/KDM7A was essential for TGF-β-induced RHOJ transcription in breast cancer cells. MKL1 interacted with and recruited KDM7A to the RHOJ promoter to cooperatively activate RHOJ transcription. KDM7A knockdown attenuated migration and invasion of breast cancer cells in vitro and mitigated the growth and metastasis of breast cancer cells in nude mice. KDM7A expression level, either singularly or in combination with that of RHOJ, could be used to predict prognosis in breast cancer patients. Of interest, KDM7A appeared to be a direct transcriptional target of TGF-β signaling. A SMAD2/SMAD4 complex bound to the KDM7A promoter and mediated TGF-β-induced KDM7A transcription. In conclusion, our data unveil a novel epigenetic mechanism whereby TGF-β regulates the transcription of the prometastatic small GTPase RHOJ. Screening for small-molecule inhibitors of KDM7A may yield effective therapeutic solutions to treat malignant breast cancers.

scholarly journals Proton Beams Inhibit Proliferation of Breast Cancer Cells by Altering DNA Methylation Status

2016 ◽  
Vol 7 (3) ◽  
pp. 344-352 ◽  
Author(s):  
Byungtak Kim ◽  
Hansol Bae ◽  
Hyunkyung Lee ◽  
Seungyeon Lee ◽  
Jeong Chan Park ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Methylation Status ◽  
Proton Beams

Inducing apoptosis effect of caffeic acid 3,4-dihydroxy-phenethyl ester on the breast cancer cells

Tumor Biology ◽  
2014 ◽  
Vol 35 (12) ◽  
pp. 11781-11789 ◽  
Author(s):  
Jiaoyuan Jia ◽  
Mei Yang ◽  
Yu Chen ◽  
Hongyan Yuan ◽  
Jinghe Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Caffeic Acid ◽  
Breast Cancer Cells

scholarly journals Epigenetic Regulation of CDH1 Is Altered after HOXB7-Silencing in MDA-MB-468 Triple-Negative Breast Cancer Cells

Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1575
Author(s):  
Ana Paço ◽  
Joana Leitão-Castro ◽  
Renata Freitas
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Epigenetic Regulation ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Methylation Status ◽  
Therapy Resistance ◽  
Migration And Invasion ◽  
A Cells

HOXB7 is often overexpressed in breast cancer cells and found to relate to poor prognosis. The search for the HOXB7 targets, as a transcription factor, has led to molecules involved in regulating cell proliferation, migration, invasion, and processes such as angiogenesis and therapy resistance. However, the specific targets affected by the deregulation of HOXB7 in breast cancer remain largely unknown in most molecular sub-types, such as triple-negative breast cancers (TNBC). To unveil the molecular basis behind these aggressive and often untreatable cancers, here we explored the contribution of HOXB7 deregulation for their aggressiveness. To this end, HOXB7 was silenced in TNBC Basal A cells MDA-MB-468, and the phenotype, gene/protein expression, and methylation profile of putative targets were analyzed. Lower migration and invasion rates were detected in HOXB7-silenced cells in comparison with the controls. In addition, these cells expressed more CDH1 and less DNMT3B, and the promoter methylation status of CDH1 diminished. Our data suggest that the HOXB7 transcription factor may act on TNBC Basal A cells by controlling CDH1 epigenetic regulation. This may occur indirectly through the up-regulation of DNMT3B, which then controls DNA methylation of the CDH1 promoter. Thus, future approaches interfering with HOXB7 regulation may be promising therapeutic strategies in TNBC treatment.

scholarly journals miR-186 Regulates the Initiation and Development of Breast Cancer via SHP-1 Methylation

2020 ◽  
Author(s):  
Kun Wang ◽  
Chunxia Zhou ◽  
Di Wang ◽  
Bin Zhang ◽  
Yongjian Zheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Promoter Region ◽  
Breast Cancer Cells ◽  
Methylation Status ◽  
Luciferase Reporter ◽  
Molecular Diagnostic ◽  
Double Labeling ◽  
Reporter Assays ◽  
Mcf 7

Abstract Background Change in the methylation status of genomic DNA, especially in CpG islands in the promoter region, is considered to be an early event in tumor initiation, leading to silencing of gene expression, subsequent abnormalities in gene structure and function, and malignant transformation of the cell. Due to the abnormal expression of miR-186 and SHP-1 in breast cancer tissues and cells, we propose that miR-186 is closely related to the methylation of SHP-1Method Using 5-azacytidine as a de-methylation agent and Validating with Setylation-specific polymerase chain reaction (MSP) after treatment. Measurement of the viability of breast cancer cells using the CCK-8 method Measurement of the apoptotic rate of breast cancer cells using annexin V-FITC/PI double labeling. Cell metastasis were measured by wound healing assay. Luciferase reporter assays was used to confirm the target of MiR-186. SHP-1 and miR-186 expression was measured by RT-PCR and western blot.Results In the present study, we found that SHP-1 expression was reduced to various degrees in all 5 cell lines (UACC-812, MDA-MB-213, MDA-MB-468, SK-RB-3 and MCF-7). 5-azacytidine can remove the methylation from the SHP-1 promoter region. Apoptosis was observed in MCF-7 cells after demethylation of the SHP-1 gene promoter region by 5-azacytidine, and the effect was time- and concentration-dependent. Luciferase reporter assays showed that miR-186 promotes methylation through binding with the 3’ UTR of the SHP-1 promoter region.Western blot showed miR-186 regulates the initiation and development of tumor cells through the SHP-1-JAK-STAT axis. In animal models, low expression of miR-186 can cause significantly limited tumor growth.Conclusion The low SHP-1 expression may be an important factor in the initiation of breast cancer, and that miR-186 could serve as an excellent molecular diagnostic marker and a possible therapeutic target.

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