T47D shNT versus T47D shRON
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ABSTRACT:
PROVIDER: PRJNA682172 | ENA |
REPOSITORIES: ENA
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Project description:Introduction: HGFL-Ron signaling is augmented in human breast cancer and is associated with poor overall prognosis. Here, we investigate the role of HGFL-Ron signaling in RON-modulated human luminal A breast cancer cells T47D through RNA-sequencing, focusing on the impact of Ron knockdown through a short hairpin construct. Methods: non-targeting shRNA (shNT) and RON-targeting shRNA (shRON) were submitted for transcriptomic characterization on the Illumina HiSeq 2500. High quality reads were aligned to the hg19 genome and quantified to generate RPKM
2020-12-03 | GSE162532 | GEO
Project description:Tamoxifen is the most widely used antiestrogen in patients with estrogen receptor (ER) positive breast cancer . However, less than half of patients benefit from tamoxifen treatment and 30-50% acquire resistance and the disease progresses. Resistance to tamoxifen is a serious problem in breast cancer therapy and major efforts are underway to find out underlying mechanisms. To find out the differential expression levels of mRNAs in tamoxifen-sensitive T47D versus tamoxifen-resistant T47D (T47DR) human breast cancer cells, T47DR (tamoxifen-resistant) cell line was established from T47D cells after the following continuous exposure to 1 μmol/L 4-Hydroxytamoxifen (H7904, Sigma, USA) for more than 6 months.Thousands of significantly different mRNA expression levels were found and analysed. Our study provides a reference data for the study of tamoxifen resistance .
2020-06-01 | GSE129544 | GEO
Project description:Differential expression levels of mRNAs in tamoxifen-sensitive T47D versus tamoxifen-resistant T47D (T47DR) human breast cancer cells
| PRJNA531696 | ENA
Project description:Purpose: The goals of this study is to compare and examine the transcriptional profile in the secondary mammospheres of control versus CIC-deficient T47D cells by mRNA sequencing and to understand the molecular basis of the CIC regulation of CSC-like properties in luminal type of breast cancer cells. Methods: DNA library for mRNA sequencing of secondary mammospheres derived from control and CIC-deficient T47D breast cancer cells was prepared using a TruSeq Stranded Total RNA LT Sample Prep Kit (Gold) and their libraries sequenced on the NovaSeq sequencer accompanying the NovaSeq 6000 S4 Reagent Kit. The trimmed reads that passed quality filters were mapped to reference genome with HISAT2, followed by assembly of transcript with StringTie. Results: A total of 20377 genes were differentially expressed (10438 upregulated and 9939 downregulated) in the CIC-deficient T47D mammospheres when compared with control mammospheres. Approximately 5% of the transcripts showed differential expression between the control and CIC-deficient secondary mammospheres, with a fold change ≥1.2 and p value <0.05. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) analyses revealed that CIC-deficient mammospheres differentially expressed genes that are involved in processes associated with cancer progression such as cell cycle, cell proliferation, cell growth, and apoptotic process, as well as autoimmunity. Conclusions: Our results show the first comparative analysis of secondary mammospheres derived from control and CIC-deficient T47D breast cancer cells. The data reported here should also provide reference for expression profiles of CSC-like cells in ER+/PR+/HER2- luminal breast cancer cells. We conclude that CIC deficiency promotes CSC-like properties and thus breast cancer progression through controlling CSC-related pathways including focal adhesion and extracellular matrix (ECM)-receptor interactions, and may also regulate cell cycle, cell proliferation, and apoptosis.
2019-12-18 | GSE142171 | GEO
Project description:RNA Sequencing Analysis of Gene Expression Profiles in Control versus CIC Knockdown T47D Mammospheres
| PRJNA596189 | ENA
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Project description:We report the comprehensive genome-wide binding peaks for key factors inovled in oxygen sensing pathways, such as HIF1α, HIF1β and EglN2. In addition, we also report the genome-wide binding peaks for NRF1 in breast cancer cells We conducted HA-EglN2, HIF1α, HIF1β (ARNT) or NRF1 ChIP-Seq in the T47D cell line that overexpresses HA-EglN2 in the presence of hypoxia (1%) and DMOG treatment. T47D parental cells treated with the same condition followed by HA ChIP-seq served as the control to filter non-specific binding.
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