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Homo sapiens

ABSTRACT: A systematic analysis of the time series gene expression in TGF-beta induced EMT by Next-generation sequencing

PROVIDER: PRJNA286131 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2056540_1.fastq.gz	Fastqsanger.gz
	SRR2056540_2.fastq.gz	Fastqsanger.gz
	SRR2056531_1.fastq.gz	Fastqsanger.gz
	SRR2056531_2.fastq.gz	Fastqsanger.gz
	SRR2056541_1.fastq.gz	Fastqsanger.gz

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A systematic analysis of the time series gene expression in TGF-beta induced EMT by Next-generation sequencing

Project description:The goal of this study is to characterize time course gene expression profiles during TGF-beta induced EMT. In particular, we aim to identify and characterize master transcription factors regulate the transition into partial-EMT state. A time series mRNA profile in A549 cells is generated from TGF-beta induced EMT samples during 0h,6h,12h,24h,36h,48h,72h and 96h by deep sequencing, in duplicate, using Illumina HiSeq 2500

2016-03-02 | E-GEOD-69667 | biostudies-arrayexpress

Gene Regulatory Circuitry of JNK Signaling Identifies Novel Regulators of Epithelial to Mesenchymal Transition

Project description:Purpose: The purpose of this study is to investigate role of JNK signaling during EMT. Method: Transcriptome of TGF-b treated NmuMG cells along with DMSO and JNKi treated NMuMG was generated using next generation high throughput sequencing in triplicates and duplicates respectively. Reads were mapped using Tophat and transcript abundance and differential expression was calculated using HTSeq-Count and DESeq programs. Results: Using time course RNA-Seq data, we uncover a large number of coding and noncoding RNAs that are modulated during stepwise progression of TGF-?-induced EMT. Concomitant with their activation behavior, Smad and JNK pathway are required for onset and progression of EMT respectively, a finding that was also confirmed in patients. Transcriptome analysis further revealed a progressive dependency of EMT on JNK signaling. Conclusion: We identified several novel transcription factors that require JNK signaling for their enhanced expression upon EMT and show that depletion of these factors during EMT hampers acquisition of transcriptional and phenotypic changes hallmark of this process. These factors are similarly induced during neurogenesis, a process also involving JNK activation and EMT. Transcriptome of TGF-b treated NmuMG cells along with DMSO and JNKi treated NMuMG was generated using next generation high throughput sequencing in triplicates and duplicates respectively.

2015-07-13 | E-GEOD-54133 | biostudies-arrayexpress

Gene Regulatory Circuitry of JNK Signaling Identifies Novel Regulators of Epithelial to Mesenchymal Transition

Project description:Purpose: The purpose of this study is to investigate role of JNK signaling during EMT. Method: Transcriptome of TGF-b treated NmuMG cells along with DMSO and JNKi treated NMuMG was generated using next generation high throughput sequencing in triplicates and duplicates respectively. Reads were mapped using Tophat and transcript abundance and differential expression was calculated using HTSeq-Count and DESeq programs. Results: Using time course RNA-Seq data, we uncover a large number of coding and noncoding RNAs that are modulated during stepwise progression of TGF-β-induced EMT. Concomitant with their activation behavior, Smad and JNK pathway are required for onset and progression of EMT respectively, a finding that was also confirmed in patients. Transcriptome analysis further revealed a progressive dependency of EMT on JNK signaling. Conclusion: We identified several novel transcription factors that require JNK signaling for their enhanced expression upon EMT and show that depletion of these factors during EMT hampers acquisition of transcriptional and phenotypic changes hallmark of this process. These factors are similarly induced during neurogenesis, a process also involving JNK activation and EMT.

2015-07-13 | GSE54133 | GEO

Gene expression in epithelial, EMT (epithelial-mesenchymal transition) and MET (mesenchymal-epithelial transition) cells

Project description:NMuMG is an epithelial cell line that can be induced into EMT by TGF-β treatment or MET by TGF-β withdrawl. During EMT, several marker genes were downregulated/upregulated, which is consistent with its mesenchymal phenotype. Transcription factors that are regulated during EMT and its reverse process MET are candidate genes for the regulations of the EMT marker genes. NMuMG cells treated with vehicle, TGF-β for 11 days, or 11days of TGF-β treatment followed by TGF-β withdrawl for another 13 days. RNA from these 3 conditions of NMuMG were extracted and subject to microarray analysis

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Project description:Epithelial-mesenchymal transition (EMT) plays a critical role in airway injury, repair, and structural remodeling. Although NFkB/RelA subnit is involved in late EMT-associated gene expression, RelA translocation is occurs later than early phases of IκB kinase (IKK)-depenedent gene expression. To investigate the hypothesis that IKK plays an independent mechanism in TGF-induced EMT, we conducted time-series proteomics and phosphoproteomics analysis of human airway epithelial cells in the absence or presence of a specific IKK inhibitor, BMS -345541.

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Gene expression profile of A549 cells treated with TGF-beta

Project description:Epithelial–mesenchymal transition (EMT) is a plastic process that converts epithelial cells into migratory and invasive cells. Accumulating evidence indicates that EMT is a key event for metastasis in several types of cancer, including non-small cell lung cancer (NSCLC). Especially, transforming growth factor-beta (TGF-beta) acts as a potent inducer of EMT and contributes to cancer progression. Emerging studies suggest that a metabolic reprograming is essential to acquire the EMT phenotype in cancer cells. However, a comprehensive understanding of metabolism in cancer EMT remains largely unexplored. Here, we analyzed metabolic changes during TGF-beta-induced EMT in NSCLC A549 cells using capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS). At the same time, we examined the expression of metabolic-related genes using microarray analysis.

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circTBRII(3-6) acts as assembly platform for IGF2BP3 protein and TBRI mRNA to enhance breast cancer cell plasticity

Project description:Transforming growth factor (TGF)-β signaling is a key driver to induce epithelial-to-mesenchymal transition (EMT), a process that enhances cancer cell plasticity and metastatic potential. However, the role of circular RNAs (circRNAs) in TGF-β signaling remains largely unexplored. Here, we identify circTBRII(3-6), a circRNA derived from TGF-β type II receptor (TBRII) pre-mRNA, as a critical enhancer of TGF-β/SMAD signaling in breast cancer cells. Depletion of circTBRII(3-6) inhibits TGF-β-induced EMT, migration, and in vivo extravasation of breast cancer cells. Mechanistically, circTBRII(3-6) acts as a scaffold that facilitates the interaction between the RNA-binding protein insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) and TGF-β type I receptor (TBRI) mRNA in an N6-methyladenosine (m6A)-dependent manner, and thereby stabilizes TBRI and promotes its expression. Furthermore, IGF2BP3 knockdown reduces circTBRII(3-6)-mediated enhancement of TGF-β/SMAD signaling, as well as TGF-β-induced EMT and migration. Our findings identify circTBRII(3-6) as a novel enforcer of TGF-β/SMAD signaling at the receptor level and highlight IGF2BP3 as a critical m6A reader that mediates circTBRII(3-6)-driven breast cancer cell plasticity.

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A systematic analysis of the time series gene expression in TGF-beta induced EMT by Next-generation sequencing

2016-03-02 | GSE69667 | GEO

Analysis of conditioned media cytokine levels of breast cancer cell lines

Project description:To identify the cytokines secreted by mesenchymal-like cancer cells that activate macrophages, the cytokine profiles of conditioned media from MCF7, MCF7 induced to undergo EMT by treatment of TGF-β, TNF-α and prolonged mammosphere culture, and MDA-MB-231 cells were analyzed by RayBio® Human Cytokine Antibody Array V. 5 samples. There are 5 groups: MCF7, MCF7 induced to undergo EMT by treatment of TGF-β (TGF-β-MCF7), TNF-α (TNF-α-MCF7), prolonged mammosphere culture (MCF7M), and MDA-MB-231 cells

2013-11-01 | E-GEOD-51938 | biostudies-arrayexpress

Time Course of TGF-beta treatment of A549 lung adenocarcinoma cell line

Project description:Time Course of TGF-beta treatment of A549 lung adenocarcinoma cell line on Affymetrix HG_U133_plus_2 arrays; triplicate experiments. The goal of the experiment is to profile temporal gene expression changes during TGF-beta-induced epithelial-mesenchymal transition (EMT). During EMT cancer cells loose their epithelial specifc proteins and gain mesenchymal proteins to acquire migratory and invasive phenotype essential for metastasis. Human A549 lung adenocarcinoma cell line was treated with 5 ng/mL TGF-beta for 0, 0.5, 1, 2, 4, 8, 16, 24, and 72 h to induce EMT. The experiment was repeated 3 times. Samples were assayed using Affymetrix HG_U133_plus_2 arrays with 54675 probe-sets, using standard techniques. We provide the raw .CEL files and a supplementary Excel spreadsheet with log-transformed data and selected results from a statistical analysis.

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