E-MTAB-9667
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ABSTRACT:
PROVIDER: E-MTAB-9667 | ExpressionAtlas | 2021-01-15
REPOSITORIES: ExpressionAtlas
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Project description:Treatment with the breast cancer drug tamoxifen confers a risk of developing uterine tumors or other endometrial pathologies. Tamoxifen is a selective estrogen receptor modulator, which demonstrates tissue-specific activity although the mechanisms remain poorly understood. Both estradiol and tamoxifen act as estrogen agonists on the human uterus, and therefore have the potential to promote carcinogenicity. Estradiol and tamoxifen elicit cellular responses via the estrogen receptors (ER), which are involved in multiple signalling pathways. The effects at the molecular level are further influenced by the differential recruitment of co-factors and the presence of specific promoter motifs in target genes. In this study, ER positive (+) Ishikawa cells are used as a model to investigate the overall effect of treatment with either 17b-estradiol or 4-hydroxytamoxifen on the gene expression profiles. Keywords: Comparison of estradiol and tamoxifen on Ishikawa human uterine cells after 24h or 48h
2006-02-01 | GSE3762 | GEO
Project description:Single cell RNA-seq of human RPE1-MYCN-ER cells with treatment of EtOH (0h) or tamoxifen for 22h, 23h and 24h to activate MYCN.
| PRJEB40898 | ENA
Project description:RNA-seq of human hTERT-RPE1 and RPE1-MYCN-ER cells with treatment of EtOH (0h) or tamoxifen for 24h, 48h and 72h to activate MYCN
| PRJEB40786 | ENA
Project description:Purpose: To assess if NLK modulates ER target gene expression, we performed transcriptome sequencing following NLK inhibition or tamoxifen treatment in the BT483 or T47D-TamR cells under estrogen-deprived condition. Methods: BT483 and T47D-TamR cells were treated with NLK-specific siRNAs, or VX-702, or Tamoxifen under estrogen-deprived condition to examine the expression profile changes of ER target genes. NovaSeq 6000 S2 Reagent Kit (Illumina) was used for paired-end reads (2×150 bp) sequencing reactions. The expression changes of ER target genes following NLK inhibition are compared to their changes following tamoxifen treatment. Results: Our results show that the ER target gene expression changes following NLK silencing or VX-702 treatment correlate with their expression changes following tamoxifen treatment.
2021-01-11 | GSE141696 | GEO
Project description:Analysis of the genome-wide response of the ER:PRL-HeLa cell line to treatment with estrogen receptor ligands estradiol, 4H-tamoxifen and bisphenol-A. Total RNA obtained from ER:PRL-HeLa cells treated for 4 hours with estradiol, 4H-tamoxifen or bisphenol -A is compared to vehicle treated controls
2011-07-13 | E-GEOD-22941 | biostudies-arrayexpress
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:Gene expression profiles (RNA seq of parental MCF7 cells and tamoxifen resistant cells after ER or FOXA1 knock down and after overexpression of FOXA1 in parenatl cells).
2016-11-01 | GSE75329 | GEO
Project description:The aim of this study is to understand the role of tamoxifen in the transcription regulation of estrogen receptor positive breast cancer cells using GRO-seq experiment. ER positive MCF-7 cells was depleted with lipid hormone in stripped culture media for 4 days, and stimulated with 17-β-estradiol (100nM), 4-OH-tamoxifen (1μM), and the combination of both for 40min. Each treatment was generated in duplicates. Then nuclei was isolated and used as the starting material for GRO-seq experiments. Sequencing data was analyzed and differential gene expression analysis was performed. A rapid induction of gene expression by 17-β-estradiol was observed as previous studies reported. While also a number of genes were also up-regulated by 4-OH-tamoxifen treatment which is considered as a ER antagnist. The data strongly indicate that as a recpressor of estrogen receptor induced transcription, tamoxifen could also perform as a partial agnist at the same time.
2017-06-30 | GSE99508 | GEO
Project description:Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor M-NM-11 apoprotein. Basal proliferation persisted in estrogen-sensitive breast cancer cells grown in hormone depleted conditioned media without or with 4-hydroxytamoxifen (OH-Tam). Downregulating ER using siRNA inhibited basal proliferation by promoting cell cycle arrest. The basal expression of RARM-NM-11, the only RARM-NM-1 isoform that was expressed in breast cancer cell lines and in most breast tumors, was supported by apo-ER but was unaffected by OH-Tam. The overlapping tamoxifen-insensitive gene regulation by apo-ER and apo-RARM-NM-11 comprised activation of mainly genes promoting cell cycle and mitosis and suppression of genes involved in growth inhibition. Cells were plated at 20% confluence in low glucose phenol red free medium supplemented with 5% charcoal stripped FBS and glutamine 24h-48h prior to transfection. Treatment with vehicle, OH-Tam (100nM), or OH-Tam (500nM) was begun an additional 24h later. Cells were transfected with control siRNA, ERM-NM-1 siRNA or RARM-NM-1 siRNA.
2011-05-13 | E-GEOD-26298 | biostudies-arrayexpress
Project description:The ets transcription factor ELF5 specifies the differentiation of mammary progenitor cells to establish the milk-secreting lineage. ER- and poor prognosis basal breast cancers arise from this progenitor cell and these cancers express high levels of Elf5. Knockdown of ELF5 expression in basal breast cancer cell lines, or forced expression in luminal breast cancer cell lines, resulted in reduced cell proliferation. Transcript profiling and chromatin immunoprecipitation revealed that the transcriptional activity of ELF5 specified the gene expression patterns that distinguish basal from luminal breast cancer, including suppression of FOXA1, GATA3 and ER, key estrogen-action genes. Tamoxifen treatment of luminal MCF7 cells upregulated Elf5 expression and cells that acquired resistance to Tamoxifen became dependent on ELF5 for proliferation. ELF5 is a regulator of breast cancer cell proliferation, transcriptionally specifies the basal molecular subtype and is utilised by ER+ breast cancer cells to escape proliferative arrest caused by Tamoxifen. ChIP-Seq using an antibody to ELF5, in T47D breast carcinoma cell lines
2012-12-27 | E-GEOD-31216 | biostudies-arrayexpress