Homo sapiens strain:MCF7 Tamoxifen resistant cancer cell line
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ABSTRACT:
PROVIDER: PRJNA1021154 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26189145_1.fastq.gz | Fastqsanger.gz | |||
| SRR26189145_2.fastq.gz | Fastqsanger.gz | |||
| SRR26189146_1.fastq.gz | Fastqsanger.gz | |||
| SRR26189146_2.fastq.gz | Fastqsanger.gz | |||
| SRR26189147_1.fastq.gz | Fastqsanger.gz |
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Project description:ChIP sequencing of FOXA1 in MCF7 cells and tamoxifen resistant MCF7 cells
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Project description:Tamoxifen, an antagonist to estrogen receptor (ER), is a first line drug used in breast cancer treatment. However, this therapy is complicated by the fact that a substantial number of patients exhibit either de novo or acquired resistance. To characterize the signaling mechanisms underlying the resistance to tamoxifen, we established a tamoxifen-resistant cell line by treating the MCF7 breast cancer cell line with tamoxifen for over 6 months. We showed that this cell line exhibited resistance to tamoxifen both in vitro and in vivo. In order to quantify the phosphorylation alterations associated with tamoxifen resistance, we performed SILAC-based quantitative phosphoproteomic profiling on the resistant and vehicle-treated sensitive cell lines where we identified >5,600 unique phosphopeptides. We found phosphorylation levels of 1,529 peptides were increased (>2 fold) and 409 peptides were decreased (<0.5-fold) in tamoxifen resistant cells compared to tamoxifen sensitive cells. Gene set enrichment analysis revealed that focal adhesion pathway was the top enriched signaling pathway activated in tamoxifen resistant cells. We observed hyperphosphorylation of the focal adhesion kinases FAK1 and FAK2 in the tamoxifen resistant cells. Of note, FAK2 was not only hyperphosphorylated but also transcriptionally upregulated in tamoxifen resistant cells. Suppression of FAK2 by specific siRNA knockdown could sensitize the resistant cells to the treatment of tamoxifen. We further showed that inhibiting FAK activity using the small molecule inhibitor PF562271 repressed cellular proliferation in vitro and tumor formation in vivo. More importantly, our survival analysis revealed that high expression of FAK2 significantly associated with short metastasis-free survival of ER-positive breast cancer patients treated with tamoxifen-based hormone therapy. Our studies suggest that FAK2 is a great potential target for the development of therapy for the treatment of hormone refractory breast cancers.
2016-05-25 | PXD001812 | Pride
Project description:Tamoxifen is the most widely administered adjuvant first-line hormone therapy for Estrogen receptor α (ERα) positive breast cancer patients. However, one from three patients will develop resistance, while the underlying molecular mechanisms are currently unclear. Recent studies reported that abnormal expression of miRNAs played a role in cancer progress. To study the potential function of miRNAs in tamoxifen resistance, Affymetrix GeneChip® miRNA 3.0 microarray was employed to identify differentially expressed miRNAs between tamoxifen sensitive MCF7 parent (MCF7-Pa) cells and induced resistant (MCF7-Re) cells.
2015-03-07 | GSE66607 | GEO
Project description:Estrogen signaling pathway is critical for breast cancer development and has remained the major adjuvant therapeutic target for this disease. Tamoxifen has been used in clinic for many years to treat ER-positive breast cancer. However a great many (30%) suffer relapse due to drug resistance. In this study, the bromodomain inhibitor JQ1 was found to down-regulate ERalpha gene expression and have anti-tumor effect in cultured tamoxifen-resisant breast cancer cells. We used microarrays to detail the global programme of gene expression in tamoxifen-resistant MCF7 cells treated with the bromodomain inhibitor JQ1. Tamoxifen-resistant breast cancer MCF7 cells were treated with DMSO (vehicle) or JQ1 (0.2 uM) for 24 hours before total RNA was purified for microarray. Each sample was triplicated.
2014-03-01 | E-GEOD-49124 | biostudies-arrayexpress
Project description:Transcriptomic profiles of MCF7-derived tamoxifen resistant cell lines
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Project description:Estrogen signaling pathway is critical for breast cancer development and has remained the major adjuvant therapeutic target for this disease. Tamoxifen has been used in clinic for many years to treat ER-positive breast cancer. However a great many (30%) suffer relapse due to drug resistance. In this study, the bromodomain inhibitor JQ1 was found to down-regulate ERalpha gene expression and have anti-tumor effect in cultured tamoxifen-resisant breast cancer cells. We used microarrays to detail the global programme of gene expression in tamoxifen-resistant MCF7 cells treated with the bromodomain inhibitor JQ1.
2014-03-01 | GSE49124 | GEO
Project description:We report the ER alpha regulatory network of Tamoxifen resistance MCF7 cell line using the Chromatin immunoprecipitated high-throughput sequencing technology (ChIP-seq). By Integrating the gene expression data (previously reported) with the ChIP-seq data, we generated ER alpha regulatory network and pathways. For ER alpha regulatory network, hub TFs with enriched motifs were identified from ER alpha peak together with PolII peaks. We then scan the position weight matrix (PWM) of ER alpha peak region of certain gene to find out the regulatory relationship between hub TF and normal TF. For regulatory pathway, genes were grouped base on their expression value at 4 different time point. Then the hub TF that plays important role in each time point of each group was identified. This study provides a framework for the application of ChIP-seq and gene expression data for the construction of ER alpha regulatory network. 4 different ChIP-seq dataset in Tamoxifen resistance MCF7 cell line
2010-12-20 | E-GEOD-26083 | biostudies-arrayexpress
Project description:Targeting the estrogen signaling pathway has proved to be of great value in the treatment of human breast cancer. Tamoxifen, a selective estrogen receptor modulator (SERM), is the most widely used antiestrogen. However, only 40-50% of patients with estrogen receptor (ER) positive breast cancer benefit from tamoxifen treatment and 30-50% acquire resistance and the disease progresses. Continuous treatment with conventional therapy may contribute to cancer progression in recurring cancers through the accumulation of drug resistant cancer progenitors. We found that MCF7 tamoxifen-resistant (TAM-R) cells possess a significantly higher proportion of cancer progenitor cells than tamoxifen-sensitive MCF7 cells. Our results indicate that the chemokine receptor CXCR4 plays an important role in the maintenance of cancer progenitors in a tamoxifen-resistant cell line and downregulation of CXCR4 signaling by small molecule antagonists specifically inhibits growth of a stem-like cell population in tamoxifen-resistant tumors both in vitro and in vivo. Whole genome gene expression analysis revealed aryl hydrocarbon receptor (AhR) signaling as one of the top networks that is differentially regulated in MCF7(TAM-R) xenograft tumors treated with the CXCR4 antagonist AMD3100 as compared to MCF7 tumors. Further, small molecule antagonists of AhR signaling specifically inhibit the progenitor population in MCF7(TAM-R) cells suggesting that the aryl hydrocarbon receptor could be a putative target for the treatment of tamoxifen-resistant breast cancers. Introduction transplants remains limited by the ability to expand these cells ex vivo. An unbiased screen with primary human HSCs identified a purine derivative, StemRegenin 1 (SR1), that promotes the ex vivo expansion of CD34+ cells. Culture of HSCs with SR1 led to a 50-fold increase in cells expressing CD34 and a 17-fold increase in cells that retain the ability to engraft immunodeficient mice. Mechanistic studies show that SR1 acts by antagonizing the aryl hydrocarbon receptor (AHR). The identification of SR1 and AHR modulation as a means to induce ex vivo HSC expansion should facilitate the clinical use of HSC therapy.
2012-12-21 | GSE31831 | GEO
Project description:Purpose: Tamoxifen is the most commonly used antiestrogen drug for breast cancer treatment, however, acquired resistance is a considerable challenge in clinic. Complexity and redundancy in biological system implies tamoxifen resistance is associated with complex biological processes. The aim of this study is to attempt to reveal the mechanism of tamoxifen resistance using high-throughput sequencing technique. Methods: We applied digital gene expression (DGE), RNA-seq, Small RNA-seq, bisulifte-seq (reduced representation bisuflite sequencing (RRBS)) with Illumina sequencing platforms, and Array CGH to analyze two well-established tamoxifen resistant cell line models: one is the LCC cell line model that was derived from MCF-7 breast cancer cell line and developed tamoxifen resistance following a step-wise strategy. This cell line model includes LCC0 (estrogen-dependent and tamoxifen sensitive), LCC1 (estrogen-independent and tamoxifen sensitive), LCC2 (derived from LCC1 with increased small-dosage tamoxifen treatment, estrogen-independent, and tamoxifen-resistant), and LCC9 (derived from LCC1 with increased small-dosage fluvestrant treatment, estrogen-independent, and cross-resistance to both fluvestrant and tamoxifen). The other is the TAMR cell line model that was derived from MCF-7 breast cancer cell line and developed four tamoxifen-resistant sublines following the strategy of high-dosage of tamoxifen treatment. Each subline was developed from the survived single cell after the tamoxifen treatment. Results: The DGE and RNA-seq results showed characteristic expression features for the both cell line models, for instance, high expression of SOX2 and alterations of other SOX gene family members, decreased expression of PGR, PTEN, TP53, EZH2, SMAD3, TGF-β1, DNMT1, APOBEC3B, FOXO3 and FOXO4, and increased expression of CDH1, APOBEC3H, FOXA1, TET2, TET3, TDG, MBD4, DNMT3a and DNMT3b between the tamoxifen-resistant cell lines with their matched parental cell lines. Small RNA seq showed the decreased expressions of miR-1, miR-196-3p, miR-18a-5p, miR-125b-5p, and the increased expression of miR-23a-3p, miR-26b-5p, miR-320d, miR-141-3p, miR-23a-3p, miR-30a-5p, miR-9-5p, miR-200c, miR-129-5p, miR-125b-5p, miR-1285-3p and miR-30b-5p between the tamoxifen-resistant cell lines and their matched parental cell lines. Additionally, let-7a and let-7c have been found to present high expression levels in the tamoxifen resistant cells in the both cell line models, even it showed significantly decreased in some TAMR cells compared with their parental cell line. The RRBS showed similar DNA methylation levels between the LCC cell lines. Array CGH showed a small number of copy number variants between the LCC cell lines. Conclusion: Our present study suggests the development of tamoxifen resistance is associated with a dynamic process of cell fate changing. Therefore, new therapeutic method that targets whole cell system and cell fate dynamics, will be a promising strategy.
2018-06-01 | GSE55380 | GEO