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SRX4203001: GSM3188536: TMX-treated rep1; Homo sapiens; RNA-Seq
1 ILLUMINA (Illumina HiSeq 2000) run: 31.4M spots, 8.5G bases, 3.3Gb downloads

Submitted by: NCBI (GEO)
Study: Tamoxifen-induced apoptosis of MCF-7 cells via GPR30/PI3K/MAPKs interactions: Verification by ODE modeling and RNA sequencing
show Abstracthide Abstract
Tamoxifen (Nolvadex) is one of the most widely used and effective therapeutic agent for breast cancer. It benefits nearly 75% of patients with ER-positive breast cancer that receive this drug. Its effectiveness is mainly attributed to its capacity to function as an estrogen receptor (ER) antagonist, blocking estrogen binding sites on the receptor, and inhibiting the proliferative action of the receptor-hormone complex. Although, tamoxifen can induce apoptosis in breast cancer cells via upregulation of pro-apoptotic factors, it can also promote uterine hyperplasia in some women. Thus, tamoxifen as a multi-functional drug could have different effects on cells based on the utilization of effective concentrations or availability of specific co-factors. Evidence that tamoxifen functions as a GPR30 (G-Protein Coupled Receptor 30) agonist activating adenylyl cyclase and EGFR (Epidermal Growth Factor Receptor) intracellular signaling networks, provides yet another means of explaining the multi-functionality of tamoxifen. Here ordinary differential equation (ODE) modeling, RNA sequencing and real time qPCR analysis were utilized to establish the necessary data for gene network mapping of tamoxifen-stimulated MCF-7 cells, which express the endogenous ER and GPR30. The gene set enrichment analysis and pathway analysis approaches were used to categorize transcriptionally upregulated genes in biological processes. Of the 2,713 genes that were significantly upregulated following a 48 h incubation with 250 µM tamoxifen, most were categorized as either growth-related or pro-apoptotic intermediates that fit into the Tp53 and/or MAPK signaling pathways. Collectively, our results display that the effects of tamoxifen on the breast cancer MCF-7 cell line are mediated by the activation of important signaling pathways including Tp53 and MAPKs to induce apoptosis. Overall design: Gene expression analysis between tamoxifen-treated MCF-7 cells and untreated MCF-7 cells.
Sample: TMX-treated rep1
SAMN09405272 • SRS3412724 • All experiments • All runs
Organism: Homo sapiens
Library:
Instrument: Illumina HiSeq 2000
Strategy: RNA-Seq
Source: TRANSCRIPTOMIC
Selection: cDNA
Layout: PAIRED
Construction protocol: Total RNA was extracted from the cells using TriPure Isolation Reagent (Roche Diagnostics GmbH, Germany) according to the kit's protocol. To avoid genomic DNA contamination, the RNA samples were treated with DNase for one hour. Following RNA isolation, creation of an RNA-seq library is the next step in transcriptome sequencing. The preparation of intended cDNA libraries and paired-end sequencing were performed by the Beijing Genome Institute (BGI), China. In total, four cDNA paired-end libraries were generated for transcriptome sequencing on Illumina HiSeq 2000 platform. Briefly, rRNA depletion methods were used for library construction. Based on the protocol, after rRNA depletion all other RNAs with or without the polyA sequence were subjected to adaptor ligation. The adapter-ligated templates were purified by the Agencourt AMPure SPRI beads and fragments with insert size about 200 bp were excised and used to synthesize the first strand cDNA.
Experiment attributes:
GEO Accession: GSM3188536
Links:
Runs: 1 run, 31.4M spots, 8.5G bases, 3.3Gb
Run# of Spots# of BasesSizePublished
SRR730056731,352,4528.5G3.3Gb2018-06-15

ID:
5689945

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