Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

E-cadherin and EMT regulation by E47 transcription represor

ABSTRACT: Expression profile analysis in MDCK-E47 cells in comparisom with MDCK CMV control cells Keywords: Genetic Modification (overexpression of E-cadherin repressors) The Oncochip microarray platform v1.1 contains 9,726 clones corresponding to 6,386 different genes, and it includes 2,489 duplicate clones. Duplicate samples (different extrations of RNA) were labeled with dUTP-Cy5 and hybridized against dUTP-Cy3-MDCK control cells. In addittion, one RNA extraction was labelled with dUTP-Cy3 and was hybridized againts dUTP-Cy5- CMV control cells

ORGANISM(S): Canis lupus familiaris

SUBMITTER: VERONICA SOBRADO

PROVIDER: E-GEOD-9147 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The class I bHLH factors E2-2A and E2-2B regulate EMT.

Sobrado Verónica R VR Moreno-Bueno Gema G Cubillo Eva E Holt Liam J LJ Nieto M Angela MA Portillo Francisco F Cano Amparo A

Journal of cell science 20090401 Pt 7

Functional loss of the cell-cell adhesion molecule E-cadherin is an essential event for epithelial-mesenchymal transition (EMT), a process that allows cell migration during embryonic development and tumour invasion. In most carcinomas, transcriptional repression has emerged as the main mechanism responsible for E-cadherin downregulation. Here, we report the identification of class I bHLH factor E2-2 (TCF4/ITF2) as a new EMT regulator. Both isoforms of E2-2 (E2-2A and E2-2B) induce a full EMT whe ...[more]

PMID: 19295128

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Project description:Loss of expression of the cell-cell adhesion molecule E-cadherin is an essential event for epithelial-mesenchymal transition (EMT), a process that allows cell migration in the developing embryo and during tumour invasion. Transcriptional repression has emerged as the main mechanism responsible for E-cadherin downregulation in most carcinomas. Recently, we have identified the class I HLH transcriptional regulator E2-2 (ITF2), in a yeast one hybrid screen designed to identify transcriptional repressors interacting with the E-pal element of the murine E-cadherin promoter. The E2-2 gene codifies two isoforms that differ in their N-terminal regions but their specific functions remain unknown. In the present work we show that both E2-2A and E2-2B induce a complete EMT, in MDCK cells, with loss of E-cadherin expression, gain of mesenchymal markers and acquisition of motile and invasive properties. Although both isoforms repress E-cadherin promoter in MDCK cells, only the E2-2B isoform does it in other epithelial cell lines. Notably, we found that E2-2B is upregulated at the mRNA level in MDCK cells after treatment with TGF-ï¢1, a key regulator of EMT. Upregulation of E2-2A/B factors was confirmed in MDCK cells overexpressing other EMT inducers, Snai1, Snai2 or E47. Interestingly, gene profiling studies indicate that bHLH E2-2 factors induce similar, yet distinct, genetic programs from those induced by bHLH E47 in MDCK cells. These results, together with the expression pattern observed in early mouse embryos, support a new role for E2-2A/B in E-cadherin regulation and EMT, and suggest an interesting interplay between bHLH factors and other E-cadherin repressors. Keywords: Genetic Modification (overexpression of E-cadherin repressors) The Oncochip microarray platform v2.0 contains 13,824 clones printed by duplicate corresponding to 9,300 different genes. Each of the MDCK transfectants (E22A, E22B) were labeled with dUTP-Cy5 and hybridized against the dUTP-Cy3-labeled MDCK-CMV controls. One additional hybridizations using reciprocal fluorochrome labeling were performed (dye-swap) in each clone. Thus, a total of two hybridizations were performed for each condition.

Dataset Information

E-cadherin and EMT regulation by E47 transcription represor

Publications

The class I bHLH factors E2-2A and E2-2B regulate EMT.

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