Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA112479 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we performed chromatin immunoprecipitation with Irf1-specific antibodies in NMuMG cells treated for 2 days with TGFbeta or left untreated (0d TGFbeta). Intersection with RNA-sequencing after downregulation of Irf1 with or without treatment with TGFbeta for two days revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.
2022-03-18 | GSE141501 | GEO
Project description:To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we downregulated Irf1 by siRNA and analyzed differentially regulated genes and pathways upon EMT induction (2 days TGFbeta) or in the absence of EMT (0 day TGFbeta). Intersection with Irf1 ChIP-sequencing after 2 days of TGFbeta treatment or in untreated cells revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.
2022-03-18 | GSE141500 | GEO
Project description:Gene expression from NMuMG cells overexpressing major satellite treated with TGFbeta
| PRJNA213208 | ENA
Project description:We have identified the transcription factor forkhead box protein F2 (Foxf2) to be upregulated in its expression during the EMT process and studied its functional contribution to EMT by siRNA-mediated knockdown in NMuMG cells treated for 4 days with TGFbeta followed by mRNA-sequencing. Our analysis revealed a dual role of Foxf2 during TGFbeta-induced EMT in promoting apoptosis while inducing cell junction breakdown and migration.
2018-10-09 | GSE112796 | GEO
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 TGFβ 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 TGFβ treatment, cells were cultured in low serum medium (0.5%) overnight followed by treatment with 5 ng/ml TGF-β1 or TGF-β3 (Sigma). After 24 hr, RNA and protein were harvested for microarray hybridization or biochemical analysis.
2009-01-13 | E-GEOD-13986 | biostudies-arrayexpress
Project description:Analysis of NMuMG cells expressing Osr2 or treated with TGF-ß. Results provide insight into a novel function of Osr2 in EMT induction.
2022-05-10 | GSE180471 | GEO
Project description:Timecourse of doxycycline induction in bitransgenic MTB/TAN, MTB/TOM, and MTB/TWNT1 mice or monotransgenic MTB control mice
| PRJNA219453 | ENA
Project description:Background To identify the spectrum of malignant attributes maintained outside the host environment, we have compared global gene expression in primary breast tumors and matched short-term epithelial cultures. Results In contrast to immortal cell lines, a characteristic 'limited proliferation' phenotype was observed, which included over expressed genes associated with the TGFbeta signal transduction pathway, such as SPARC, LOXL1, RUNX1, and DAPK1. Underlying this profile was the conspicuous absence of hTERT expression and telomerase activity, a significant increase in TGFbeta receptor2, its cognate ligand, and the CDK inhibitor, p21CIP1/WAF1. Concurrently, tumor tissue and primary cultures displayed low transcript levels of proliferation-related genes, such as, TOP2A, ANKT, RAD51, UBE2C, CENPA, RRM2, and PLK. Conclusions Our data demonstrate that commonly used immortal cell lines do not reflect some aspects of tumor biology as closely as primary tumor cell cultures. The gene expression profile of malignant tissue, which is uniquely retained by cells cultured on solid substrates, could facilitate the development and testing of novel molecular targets for breast cancer.
2005-11-03 | E-SMDB-2888 | biostudies-arrayexpress
Project description:TGFβ ligands act as tumor suppressors in early stage tumors but are paradoxically diverted into potent prometastatic factors in advanced cancers. The molecular nature of this switch remains enigmatic. We now show that TGFβ-dependent cell migration, invasion and metastasis are empowered by mutant-p53. To investigate the specific gene expression program by which mutant-p53 and TGFβ control invasion and metastasis in breast cancer cells, we compared the TGFβ transcriptomic profile of control and mutant-p53 depleted MDA-MB-231 cells. Experiment Overall Design: MDA-MB-231 cells, stably expressing either control (shGFP) or anti-p53 (shp53) short-hairpin RNAs, were left untreated or treated with TGFbeta. Samples were then processed for total RNA extraction and hybridization on Affymetrix microarrays. Four biological replicas (A, B, C, D) were used for each of the 4 conditions (1: untreated control; 2: TGFbeta treated control; 3: untreated p53-depleted cells; 4: TGFbeta treated mutant-p53-depleted cells), for a total of 16 samples.
2009-04-11 | E-GEOD-14491 | biostudies-arrayexpress