Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A TGF-β-induced long non-coding RNA eSNAI1 activates SNAI1 enhancer in cis and stimulates epithelial to mesenchymal transition of cancer cells

ABSTRACT: A TGF-β-induced long non-coding RNA eSNAI1 activates SNAI1 enhancer in cis and stimulates epithelial to mesenchymal transition of cancer cells

PROVIDER: PRJNA1145363 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR30168000_1.fastq.gz	Fastqsanger.gz
	SRR30168000_2.fastq.gz	Fastqsanger.gz
	SRR30168001_1.fastq.gz	Fastqsanger.gz
	SRR30168001_2.fastq.gz	Fastqsanger.gz
	SRR30168002_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

A TGF-ß-induced cis-regulatory long non-coding RNA eSNAI1 activates SNAI1 enhancer and stimulates epithelial-to-mesenchymal transition of cancer cells [CRISPR screen, activation]

Project description:Transforming growth factor-β (TGF-β) signaling stimulates cell movement and plasticity by inducing epithelial-to-mesenchymal transition (EMT). This process is aberrantly activated in cancer and facilitates tumor cell migration, invasion, metastasis, and therapy resistance. In this study, we identified the lncRNA eSNAI1 (SCREEM2) as a potent activator of TGF-β/SMAD signaling and SNAI1 expression. eSNAI1 depletion reduces TGF-β-induced EMT, migration, in vivo extravasation, stemness, and chemotherapy resistance of breast cancer cells. eSNAI1 promotes TGF-β/SMAD signaling by inhibiting TGF-β type I receptor polyubiquitination and proteasomal degradation. eSNAI1 stimulates the expression of the nearby gene SNAI1, which encodes the EMT transcription factor SNAI1 that facilitates TGF-β/SMAD signaling by retaining the inhibitory SMAD7 in the nucleus. Mechanistically, eSNAI1 acts as an enhancer RNA (eRNA) to potentiate SNAI1 expression through in-cis regulation. Furthermore, we uncovered that eSNAI1 interacts with and reinforces the binding of the co-activator bromodomain-containing protein 4 (BRD4) to the H3 lysine 27 acetylation (H3K27ac)-enriched SNAI1 enhancer region. Our findings identify eSNAI1 as a potent activator of TGF-β signaling and a promising therapeutic target to mitigate overactive TGF-β signaling and EMT in cancer cells.

2025-03-06 | GSE276203 | GEO

A TGF-β-induced long non-coding RNA eSNAI1 activates SNAI1 enhancer in cis and stimulates epithelial to mesenchymal transition of cancer cells

Project description:We identified a tumor-promoting long non-coding RNA (lncRNA) named eSNAI1 (enhancer RNA of SNAI1) which is induced by TGF-beta and enforces TGF-beta signaling. It was found to promtotes TGF-beta-induced epithelial-to-mesenchymal transition (EMT), cell migration and extravasation in a zebrafish exnograft model. To better dissect the downstream target genes and elucidate the signaling pathways altered by eSNAI1, we overexpressed eSNAI1 by CRISPRa in MDA-MB-231 cells. Total RNA was collected and sent for RNA sequencing analysis. Afterwards, differentially expressd genes were used for the pathway enrichment analysis and gene set enrichment analysis (GSEA).

2025-03-06 | GSE274181 | GEO

A TGF-ß-induced cis-regulatory long non-coding RNA eSNAI1 activates SNAI1 enhancer and stimulates epithelial-to-mesenchymal transition of cancer cells [CRISPR screen, activation]

Project description:A TGF-ß-induced cis-regulatory long non-coding RNA eSNAI1 activates SNAI1 enhancer and stimulates epithelial-to-mesenchymal transition of cancer cells [CRISPR screen, activation]

| PRJNA1155681 | ENA

Identification of a SNAI1 enhancer RNA that drives cancer cell plasticity

Project description:Enhancer RNAs (eRNAs) are a pivotal class of enhancer-derived non-coding RNAs that drive gene expression. Here we identify the SNAI1 enhancer RNA (SNAI1e; SCREEM2) as a key activator of SNAI1 expression and a potent enforcer of transforming growth factor-β (TGF-β)/SMAD signaling in cancer cells. SNAI1e depletion impairs TGF-β-induced epithelial-mesenchymal transition (EMT), migration, in vivo extravasation, stemness, and chemotherapy resistance in breast cancer cells. SNAI1e functions as an eRNA to cis-regulate SNAI1 enhancer activity by binding to and strengthening the enrichment of the transcriptional co-activator bromodomain-containing protein 4 (BRD4) at the local enhancer. SNAI1e selectively promotes the expression of SNAI1, which encodes the EMT transcription factor SNAI1. Furthermore, we reveal that SNAI1 interacts with and anchors the inhibitory SMAD7 in the nucleus, and thereby prevents TGF-β type I receptor (TβRI) polyubiquitination and proteasomal degradation. Our findings establish SNAI1e as a critical driver of SNAI1 expression and TGF-β-induced cell plasticity.

2025-03-06 | GSE274882 | GEO

ChIP-sequencing of Snai1 transcription factor in triple negative breast cancer cell line Hs578T

Project description:This experiment is performed to reveal the novel binding sites of Snai1 transcription factor globally in triple negative breast cancer cell line Hs578T. We also reveal the effect of TGF cytokine on the binding sites of Snai1.

2018-04-25 | E-MTAB-5242 | biostudies-arrayexpress

Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells

Project description:To investigate the effect of SNAI1 Knockout on development and growth of triple-negative human breast cancer cells The transcription factor SNAI1 mediates epithelial-mesenchymal transition, fibroblast activation and controls inter-tissue migration. High SNAI1 expression characterizes metastatic triple-negative breast carcinomas, and its knockout by CRISPR/Cas9 uncovered establishment of an epithelio-mesenchymal phenotype accompanied by reduced signaling by the cytokine TGF-β. The SNAI1 knockout cells exhibited plasticity in differentiation, drifting towards the luminal phenotype, gained stemness potential and could differentiate into acinar mammospheres in 3D culture. Loss of SNAI1 derepressed the transcription factor FOXA1, a pioneering factor of mammary luminal progenitors. FOXA1 induced a specific gene program, including the androgen receptor (AR). Inhibiting AR via a specific antagonist regenerated the basal phenotype and blocked acinar differentiation. Thus, loss of SNAI1 in the context of triple-negative breast carcinoma cells promotes an intermediary luminal progenitor phenotype that gains differentiation plasticity, based on the dual transcriptional action of FOXA1 and AR. This function of SNAI1 provides means to separate cell invasiveness from progenitor cell de-differentiation as independent cellular programs.

2022-10-01 | GSE210870 | GEO

RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

Project description:In skeletal myogenesis, the transcription factor MyoD, activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snai1/2-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snai1/2 does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1/2-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail1/2- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells. In vivo depletion of transcription factor with siRNA followed by whole transcriptome analysis (RNA-seq) to identify target genes.

2012-07-04 | E-GEOD-38236 | biostudies-arrayexpress

RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

2012-07-05 | GSE38236 | GEO

TGF-β1 activates neutrophil signaling and transcription but not migration

Project description:TGF-β1 activates neutrophil signaling and transcription but not migration

| PRJNA961203 | ENA

H4K16ac activates retrotransposons and contributes to their cis regulatory function

Project description:H4K16ac activates retrotransposons and contributes to their cis regulatory function

| PRJNA826517 | ENA