Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA139541 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Smad2/3 binding regions in mouse mammary gland epithelial cells (NMuMG) treated with TGF-beta for 1.5 h were determined by ChIP-seq to evaluate the transcriptional mechanism of TGF-beta-Smad signaling.
2019-08-29 | GSE121254 | GEO
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
Project description:TGF-beta is one of the most important cytokines that induce epithelial to mesenchymal transition (EMT). In this dataset, we examined TGF-beta induced changes in gene and exon level expression. Core probesets of two samples were analyzed. NMuMG cells were stimulated with TGF-beta for 24 h or left untreated.
2011-11-01 | E-GEOD-28184 | biostudies-arrayexpress
Project description:Response of mouse mammary epithelial cells NMuMG to TGF-b1 - time course experiment. Identification of novel gene targets involved in TGF-b1-driven regulation of epithelial-mesenchymal transition (EMT).
2004-10-01 | E-MEXP-139 | biostudies-arrayexpress
Project description:Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) facilitate breast cancer (BC) metastasis, however stable molecular changes that result as a consequence of these processes remain poorly defined. Therefore, we sought to identify molecular markers that could distinguish tumor cells that had completed the EMT:MET cycle in the hopes of identifying and targeting unique aspects of metastatic tumor outgrowth.Therefore, normal murine mammary gland (NMumG) cells transformed by overexpression of EGFR (NME) cells were cultured in the presence of TGF-beta1 (5 ng/ml) for 4 weeks, at which point TGF-beta1 supplementation was discontinued and the cells were allowed to recover for an additional 4 weeks (Post-TGF-Rec). Total RNA was prepared from unstimulated cells (Pre-TGF) of similar passage and compared by microarray analysis. The two groups were analyzed in triplicate, three Pre-TGF samples and three Post-TGF-Rec samples.
2014-01-30 | E-GEOD-54491 | biostudies-arrayexpress
Project description:We identified RNA binding motif protein 47 (RBM47) as a target gene of transforming growth factor (TGF)-beta in mammary gland epithelial cells (NMuMG cells) that have undergone the epithelial-to-mesenchymal transition (EMT). TGF-beta repressed RBM47 expression in NMuMG cells and lung cancer cell lines. Expression of RBM47 correlated with good prognosis in patients with lung, breast, and gastric cancer. RBM47 suppressed the expression of cell metabolism-related genes, which were the direct targets of nuclear factor erythroid 2-related factor 2 (Nrf2; also known as NFE2L2). RBM47 bound to KEAP1 and Cullin3 mRNAs, and knockdown of RBM47 inhibited their protein expression, which led to enhanced binding of Nrf2 to target genomic regions. Knockdown of RBM47 also enhanced the expression of some Nrf2 activators, p21/CDKN1A and MafK induced by TGF-beta. Both mitochondrial respiration rates and the side population cells in lung cancer cells increased in the absence of RBM47. Our findings, together with the enhanced tumor formation and metastasis of xenografted mice by knockdown of the RBM47 expression, suggested tumor suppressive roles for RBM47 through the inhibition of Nrf2 activity. Effect of shRNA for RBM47 and TGF-beta on gene expression was evaluated by RNA-seq and RBM47-bound RNAs were identified by RIP-seq in A549 cells.
2016-03-01 | E-GEOD-61910 | biostudies-arrayexpress
Project description:We have developed a progression series of increasingly metastatic cell lines generated from the normal mammary epithelial cell line, NMuMG, to distinguish between early changes in cancer initiation and metastasis-promoting alterations.
2017-06-17 | GSE94637 | GEO
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.
2013-07-26 | GSE48204 | GEO
Project description:Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) facilitate breast cancer (BC) metastasis, however stable molecular changes that result as a consequence of these processes remain poorly defined. Therefore, we sought to identify molecular markers that could distinguish tumor cells that had completed the EMT:MET cycle in the hopes of identifying and targeting unique aspects of metastatic tumor outgrowth.Therefore, normal murine mammary gland (NMumG) cells transformed by overexpression of EGFR (NME) cells were cultured in the presence of TGF-beta1 (5 ng/ml) for 4 weeks, at which point TGF-beta1 supplementation was discontinued and the cells were allowed to recover for an additional 4 weeks (Post-TGF-Rec). Total RNA was prepared from unstimulated cells (Pre-TGF) of similar passage and compared by microarray analysis.
2014-01-30 | GSE54491 | GEO
Project description:We report the gene expression in mouse NMuMG cells with or without UGCG depletion using RNA sequencing. After data analysis, the 11218 transcripts were identified. Among these transcripts, the TGF-β signaling target genes and EMT marker genes were significantly upregulated in UGCG depleted NMuMG cells. Then we used these genes and mouse TGF-β or EMT gene signatures to do the gene set enrichment analysis and showed the negative correlation of UGCG and TGF-β signaling or EMT in NMuMG cells.
2022-01-03 | GSE192691 | GEO