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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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ChIP-Seq of Klf4 in NMuMG normal murine mammary gland epithelial cells.

ABSTRACT: Chromatin immunoprecipitation of Klf4 in NMuMG cells identifies gene promoter sequences that are directly bound by Klf4. Chromatin immunoprecipitation using a Klf4-specific antibody in NMuMG cells followed by next generation sequencing (ChIP-Seq).

ORGANISM(S): Mus musculus

SUBMITTER: Neha Tiwari

PROVIDER: E-GEOD-49445 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Klf4 is a transcriptional regulator of genes critical for EMT, including Jnk1 (Mapk8).

Tiwari Neha N Meyer-Schaller Nathalie N Arnold Phil P Antoniadis Helena H Pachkov Mikhail M van Nimwegen Erik E Christofori Gerhard G

PloS one 20130225 2

We have identified the zinc-finger transcription factor Kruppel-like factor 4 (Klf4) among the transcription factors that are significantly downregulated in their expression during epithelial-mesenchymal transition (EMT) in mammary epithelial cells and in breast cancer cells. Loss and gain of function experiments demonstrate that the down-regulation of Klf4 expression is required for the induction of EMT in vitro and for metastasis in vivo. In addition, reduced Klf4 expression correlates with sh ...[more]

PMID: 23451207

Similar Datasets

Expression data from Klf4 KD cells in the presence and absence of TGFÎ² in NMuMG cells

Project description:Expression profiling after Klf4 KD during EMT in NMuMG reveals a significant number of genes that are transcriptionally deregulated Gene expression profiling is performed in Klf4 ablated (siKlf4) NMuMG cells. Cells transfected with siControl is used as a control. The cells were either treated with TGFÎ² (2ng/ml) or not.

2013-07-24 | E-GEOD-49151 | biostudies-arrayexpress

Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

Project description:Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFÎ²-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. Ablation of Ezh2 expression prevents EMT, while forced expression of Ezh2 restores EMT in Sox4-deficient cells. Ezh2-mediated H3K27me3 marks associate with key EMT genes, representing an epigenetic EMT signature that predicts patient survival. Our results identify Sox4 as a master regulator of EMT by governing the expression of the epigenetic modifier Ezh2. Our Dataset comprises of 12 ChIP-seq samples using chromatin from NMuMG cells which was immunoprecipitated using H3K27me3-specific antibody during TGFÎ²-induced EMT (2ng/ml) at 6 different stages (day 0, 1, 4, 7, 10, 20).

2013-06-20 | E-GEOD-45579 | biostudies-arrayexpress

Expression data from Sox4 knockdown cells in the presence and absence of TGFÎ² in NMuMG cells

Project description:Expression profiling after Sox4 knockdown (KD) during epithelial to mesenchymal transition (EMT) in NMuMG reveals a significant number of genes that are transcriptionally deregulated. Gene expression profiling is performed in Sox4-ablated (siSox4) NMuMG cells. Cells transfected with siControl is used as a control. The cells were either treated with transforming growth factor-beta (TGFÎ²; 2ng/ml) or not.

2013-06-20 | E-GEOD-44050 | biostudies-arrayexpress

ChIP-Seq of Klf4 in NMuMG normal murine mammary gland epithelial cells.

Project description:Chromatin immunoprecipitation of Klf4 in NMuMG cells identifies gene promoter sequences that are directly bound by Klf4.

2013-08-01 | GSE49445 | GEO

Klf4 is a transcriptional regulator of genes critical for EMT, including Jnk1 (Mapk8).

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-01 | E-GEOD-49451 | biostudies-arrayexpress

Expression data from Klf4 KD cells in the presence and absence of TGFβ in NMuMG cells

Project description:Expression profiling after Klf4 KD during EMT in NMuMG reveals a significant number of genes that are transcriptionally deregulated

2013-07-24 | GSE49151 | 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

2013-07-26 | E-GEOD-48204 | biostudies-arrayexpress

mRNA profiling of NMuMG mouse mammary epithelial cells transformed in vitro by long-term incubation in the presence of aluminium chloride vs controls incubated in parallel in the presence of the same dilution of solvent (H2O) alone. Referred to as \\"NMuMG series I\\" in the citing manuscript (Mandriota et al., submitted).

Project description:Salts of aluminium, a chemical element devoid of biological function, are added to many industrial products of frequent use because of aluminium's chemical versatility. As a result of lifetime exposure, aluminium accumulates in several organs including the mammary gland. At concentrations in the range of those measured in the breast of women living in industrialised countries, aluminium chloride transforms human and mouse mammary epithelial cells in vitro. These results challenge the safety commonly ascribed to aluminium and suggest that it could be a human carcinogen. NMuMG is a spontaneously immortalised, non tumorigenic mouse mammary epithelial cell line originally derived from NAMRU mice that, following chronic culture in the presence of aluminium - in the form of AlCl3 x 6H2O - becomes able to form tumors and metastasis in NOD-scid and nude mice. As a part of our investigations on the mechanisms by which aluminium might transform mammary epithelial cells, we analysed the mRNA profile of NMuMG cells transformed in vitro by aluminium or the corresponding untreated controls cultured in parallel by cDNA microarray. We used the Clariom S microarray from Thermofisher, that covers more than 20'000 well annotated mRNAs. The cell culture experiment analyzed in this microarray is referred to as \\"NMuMG series I\\" in the citing manuscript (Mandriota et al., submitted).

2020-11-30 | E-MTAB-9733 | biostudies-arrayexpress

mRNA profiling of NMuMG mouse mammary epithelial cells transformed in vitro by long-term incubation in the presence of aluminium chloride vs controls incubated in parallel in the presence of the same dilution of solvent (H2O) alone. Referred to as \"NMuMG series III\" in the citing manuscript (Mandriota et al., submitted).

Project description:Salts of aluminium, a chemical element devoid of biological function, are added to many industrial products of frequent use because of aluminium's chemical versatility. As a result of lifetime exposure, aluminium accumulates in several organs including the mammary gland. At concentrations in the range of those measured in the breast of women living in industrialised countries, aluminium chloride transforms human and mouse mammary epithelial cells in vitro. These results challenge the safety commonly ascribed to aluminium and suggest that it could be a human carcinogen. NMuMG is a spontaneously immortalised, non tumorigenic mouse mammary epithelial cell line originally derived from NAMRU mice that, following chronic culture in the presence of aluminium - in the form of AlCl3 x 6H2O - becomes transformed in vitro. In this specific experiment - referred to as NMuMG series III in the citing manuscript (Mandriota et al., submitted) - transformation was assessed in vitro, by the soft agar assay. As a part of our investigations on the mechanisms by which aluminium might transform mammary epithelial cells, we analysed the mRNA profile of NMuMG cells transformed in vitro by aluminium or the corresponding untreated controls cultured in parallel by cDNA microarray. We used the Clariom S microarray from Thermofisher, that covers more than 20'000 well annotated mRNAs.

2020-11-30 | E-MTAB-9735 | biostudies-arrayexpress

Transcription profiling of mouse NMuMG cells after MTB/TRAS short-term induction, tumor, and TGFbeta treatment

Project description:To test whether SVD regression is sufficiently sensitive to detect activation of a secondary, endogenous pathway as it occurs following ectopic manipulation of a strong primary pathway by focusing on the relationship between the Ras and TGFÎ² signaling pathways. Experiment Overall Design: Bitransgenic MTB/TRAS mice in an FVB/N background were generated by crossing MTB and TRAS mice. To induce oncogenic v-H-Ras expression, 6-week old MTB/TRAS female mice were administered 2 mg/ml doxycycline with 5% sucrose in their drinking water. Mammary tissue was harvested at different post-induction time points and snap frozen. To generate Ras-driven tumors, MTB/TRAS mice were administered 0.012 mg/ml doxycycline in their drinking water and monitored for tumor formation. Mice were sacrificed when tumors reached ~1 cm and tissue was snap frozen. The non-transformed murine mammary epithelial cell line, NMuMG, was cultured in Dulbeccoâs modified Eagleâs medium (DMEM) supplemented with 10% bovine calf serum, 1% penicillin/streptomycin, and 2 mM L-glutamine. For TGFÎ² treatment, cells were cultured in low serum medium (0.5%) overnight followed by treatment with 5 ng/ml TGF-Î²1 or TGF-Î²3 (Sigma). After 24 hr, RNA and protein were harvested for microarray hybridization or biochemical analysis.

2009-01-13 | E-GEOD-13986 | biostudies-arrayexpress

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