Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-sequencing of isogenic primary, pre-malignant immortalized, and Ras-transformed human mammary epithelial cells

ABSTRACT: RNA-sequencing of isogenic primary, pre-malignant immortalized, and Ras-transformed human mammary epithelial cells

PROVIDER: PRJNA434238 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6729601_1.fastq.gz	Fastqsanger.gz
	SRR6729601_2.fastq.gz	Fastqsanger.gz
	SRR6729602_1.fastq.gz	Fastqsanger.gz
	SRR6729602_2.fastq.gz	Fastqsanger.gz
	SRR6729603_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

RNA-sequencing of isogenic primary, pre-malignant immortalized, and Ras-transformed human mammary epithelial cells

Project description:Understanding changes in gene expression during tumor initiation and progression is critical to understanding how genetic alterations drive malignancy. We used a genetically defined cell culture model to study the progression of normal human mammary epithelial cells (HMECs) to malignancy. Primary HMECs were immortalized through the expression of hTERT, p53DD, cyclin D1, CDK4R24C and c-MYCT58A. This immortalization conferred limitless replicative potential as well as migratory capacity. These pre-malignant cells were subsequently HRASG12V transformed, which converted the immortalized cells to a fully tumorigenic state with significantly increased invasive capacity. We analyzed the cells using RNA-sequencing, and we report dramatic mRNA expression changes during the pre-malignant immortalization of primary cells, and very few mRNA expression changes occurring during oncogenic Ras transformation. RNA signatures in pre-malignant immortalized and Ras-transformed cells are consistent with previously reported epithelial-to-mesenchymal transition (EMT) signatures.

2018-05-25 | GSE110677 | GEO

Hyperactive RAS/MAPK introduces cancer-specific mitotic vulnerabilities

Project description:We performed tanscriptional profiling of ARPE19 and four isogenic transformed cells lines in which Ras or two downstream pathways, MAPK or PI3K/mTOR, were up-regulated. The purpose of this study is to understand how Ras signaling impacts kinetochore function.

2022-09-21 | GSE172512 | GEO

Proteomic analysis of 3D cultures of fibroblasts and Ras-transformed HaCaT keratinocytes

Project description:HaCaT, and its three retrovirally c-Ha-ras-transformed subclones, A5, II-4 and RT3 (abbreviated as ras-HaCaTs in the text) that exhibit benign, invasive and malignant phenotypes, respectively, were cultured as 3D monocultures and co-cultures with fibroblasts. After hypotonic lysis of the cells, the insoluble proteins were analysed by LC-MS/MS.

2019-09-10 | PXD013113 | Pride

Dynamics of chromatin accessibility during TGF-beta-induced EMT of Ras-transformed mammary gland epithelial cells [FAIRE-Seq]

Project description:We performed global mapping of accessible chromatin in mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-assisted isolation of regulatory element (FAIRE)-sequencing (seq) to analyze the mechanisms of transcriptional regulation during TGF-beta-induced EMT.

2017-04-10 | GSE69364 | GEO

Transcription profiling of mouse NIH3T3 cells were compared with myc/ras transformed NIH3T3 cells and with IRF1 expressing myc/ras transformed cells

Project description:Interferons have been ascribed to mediate antitumor effects. IRF-1 is a major target gene of interferons. It inhibits cell proliferation and oncogenic transformation. Here we show that 60% of all mRNAs deregulated by oncogenic transformation mediated by c-myc and H-ras are reverted to the expression levels of non-transformed cells by IRF-1. These include cell cycle regulating genes. Activation of IRF-1 decreases cyclin D1 expression and CDK4 kinase activity concomitant with dephosphorylation of pRb. These effects of IRF-1 are mediated by inhibition of the MEK-ERK pathway and a transcriptional repression of cyclin D1. IRF-1 mediated effects on cell cycle progression were found to be overridden by ectopic expression of cyclin D1. Ablation of cyclin D1 by RNA interference experiments prevents transformation and tumor growth in nude mice. The data demonstrate that cyclin D1 is a key target for IRF-1 mediated tumor suppressive effects. Experiment Overall Design: 3 samples were analysed, two replicates per sample. NIH3T3 cells were compared with myc/ras transformed NIH3T3 cells and with IRF1 expressing myc/ras transformed cells.

2008-06-14 | E-GEOD-6505 | biostudies-arrayexpress

FAIRE-seq analysis of Ras transformed mouse mammary gland epithelial cells transfected with Etv4 and Etv5 siRNAs and stimulated with TGF-beta.

2017-04-10 | GSE94977 | GEO

Dynamics of MBD2 deposition across methylated DNA regions during malignant transformation of human mammary epithelial cells (2)

Project description:DNA methylation is thought to induce a transcriptional silencing through the combination of two mechanisms: the repulsion of transcriptional activators that do not recognize their binding sites when methylated, and the recruitment of transcriptional repressors that specifically bind methylated DNA. Methyl CpG Binding Domain proteins MeCP2, MBD1 and MBD2 belong to the latter category. However, the exact contribution of each protein in the DNA methylation dependent transcriptional repression occurring during development and diseases remains elusive. Here we present MBD2 ChIPseq data generated from the endogenous protein in an isogenic cellular model of human mammary oncogenic transformation. In immortalized or transformed cells, MBD2 was found in one fourth of methylated regions and associated with transcriptional silencing. Depletion of MBD2 induces upregulations of genes bound by MBD2 and methylated in their transcriptional start site regions. MBD2 was partially redistributed on methylated DNA during oncogenic transformation, independently of DNA methylation changes. Genes downregulated during this transformation preferentially gained MBD2 binding sites on their promoter. Depletion of MBD2 in transformed cells induced the upregulation of some of these repressed genes, independently of the strategy used for the abrogation of oncosuppressive barriers. Our data confirm that MBD2 is a major interpret of DNA methylation, and show an unreported dynamic in this interpretation during oncogenic transformation. RNAseq of untreated HMEC-hTERT cells, siCtrl, siMBD2 or DAC treated HMLER cells, siCtrl or siMBD2 treated HME-ZEB1-RAS and HME-shP53-RAS cells, in duplicates.

2015-06-17 | E-GEOD-63234 | biostudies-arrayexpress

MNase seq data of primary, immortalized and transformed mouse skin fibdroblasts from Ssrp1fl/fl;CreERT2 mice

Project description:Nucleosome distribution was compared between primary, immortalized and transformed mouse skin fibdroblasts with and without FACT using conditional knockout of Ssrp1 subunit of FACT

2020-06-16 | GSE149951 | GEO

Differential gene expression in Ki-RAS and Ha-RAS cell lines.

Project description:Comparison of gene expression in Ha-RAS transformed cells versus untransformed Caco-2. Comparison of gene expression in Ki-RAS transformed cells versus untransformed Caco-2.

2009-04-07 | GSE12203 | GEO

Transcription profiling of human breast tumor epithelia cell types HMLER and BPLER compared to immortalized parent cells of origin - HME and BPE

Project description:The gene expression of two different tumorigenic human breast epithelial cell types (HMLER and BPLER) is compared with their immortalized parental cell-of-origin (HME and BPE). Experiment Overall Design: Two different normal primary human mammary epithelial cell populations (BPECs and HMECs) were isolated based on their differing in vitro growth requirements. These cells were immortalized by hTERT giving rise to BPE and HME cells. These hTERT immortalized cells (BPE and HME) were transformed by SV40-early region (LT+st) and H-Ras giving rise to transformed tumorigenic derivatives BPLER and HMLER. Biological replicates (4 - 6 samples) for each of 4 cell types were analyzed (untransformed hTERT immortalized cell populations (BPE&HME), and transformed tumorigenic derivatives (BPLER & HMLER).

2008-06-15 | E-GEOD-6885 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data