Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from normal murine mammary epithelial cell line NMuMG stimulated with TGF-beta

ABSTRACT: 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.

ORGANISM(S): Mus musculus

SUBMITTER: Daizo Koinuma

PROVIDER: E-GEOD-28184 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

TGF-β drives epithelial-mesenchymal transition through δEF1-mediated downregulation of ESRP.

Horiguchi K K Sakamoto K K Koinuma D D Semba K K Inoue A A Inoue S S Fujii H H Yamaguchi A A Miyazawa K K Miyazono K K Saitoh M M

Oncogene 20111031 26

Epithelial-mesenchymal transition (EMT) is a crucial event in wound healing, tissue repair and cancer progression in adult tissues. We have recently shown that transforming growth factor (TGF)-β-induced EMT involves isoform switching of fibroblast growth factor receptors by alternative splicing. We performed a microarray-based analysis at single exon level to elucidate changes in splicing variants generated during TGF-β-induced EMT, and found that TGF-β induces broad alteration of splicing patte ...[more]

PMID: 22037216

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Project description:Most available CRC cell lines have lost their TGF-beta response through the acquisition of mutations either in TGF-beta type II receptor (TGFBR2) or the intracellular mediator SMAD4 (Reviewed in Markowitz et al. 2002). To study the effect of TGF-beta in CRC epithelial cells, we restored wild-type TGFBR2 expression in the CRC cell line LS174T (LS). Ls174T cells are mutant for beta-catenin and therefore exhibit constitutive Wnt activity, which results in the expression of a genetic profile similar to that of intestinal epithelial progenitor cells (van de Wetering, Sancho et al. 2002). They thus reflect tumor cells at the initial stages of tumorogenesis. In addition, Ls174T cells bear mutations in the TGF-beta receptor II (TGFBR2) sequence at the BATRII locus (Grady and Markowitz 2002). This mutation gives rise to a non-functional truncated form of the receptor lacking the transmembrane domain and the serine-threonine kinase domain (Parsons, Myeroff et al. 1995). We generated inducible clones of Ls174T cells, where the expression of TGFBR2 could be controlled at will by the presence or absence of doxycycline (LSTGFBR2 cell line). Re-expression of wild-type receptor in Ls174T cells (LSTGFBR2) restored TGF-beta signalling resulting in strong phosphorylation of SMADs and activation of SMAD-binding reporter activity. Functionally, TGF-beta signalling in LSTGFBR2 resulted in a strong cytostatic response. By genome wide expression profiling using microarrays we investigated genes regulated by TGF-beta in this cell line. LsTGFBR2 inducible cells were generated by the Invitrogen T-Rex system following manufacturers instructions. LSTGFBR2 were seeded at 60% confluence in the presence or absence of Doxycycline and treated with TGF-M-NM-21 for 16 hours. Gene expression profiles were measured in duplicate using HG-U133 plus 2.0. We used RMA background correction, quantile normalization and RMA summarization (Gautier et al., 2004). A TGF-M-NM-2 response signature was obtained by selecting genes with limma P-value < 0.05 and at least two fold up-regulation in TGF-M-NM-2 treated LSTGFBR2 cells.

Dataset Information

Expression data from normal murine mammary epithelial cell line NMuMG stimulated with TGF-beta

Publications

TGF-β drives epithelial-mesenchymal transition through δEF1-mediated downregulation of ESRP.

Similar Datasets

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