Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

RNA-seq of canine MDCK epithelial cell line compared to cell line overexpressing ERK2 or cell line with conditional activation of the ERK pathway

ABSTRACT: Using RNA-seq and canine MDCK epithelial cells, we analyzed mRNA expression profiles of cells overexpressing ERK2 and cells where the ERK pathway was activated for 24 hrs. For this purpose, three cell lines were used: parental MDCK cells, MDCK cells overexpressing FLAG-ERK2 or MDCK cells expressing conditionally active Raf protein (ΔRaf1:ER). Activation of the ERK pathways was achieved by the addition of 4-Hydroxytamoxifen that converts ΔRaf1:ER protein to the active form and it subsequently activates the ERK pathway.

INSTRUMENT(S): Illumina HiSeq 2000

ORGANISM(S): Canis lupus familiaris

SUBMITTER: Jan Rasl

PROVIDER: E-MTAB-12132 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

ERK2 signaling regulates cell-cell adhesion of epithelial cells and enhances growth factor-induced cell scattering.

Rasl Jan J Grušanović Josipa J Klímová Zuzana Z Čáslavský Josef J Groušl Tomáš T Novotný Jiří J Kolář Michal M Vomastek Tomáš T

Cellular signalling 20220804

The ERK signaling pathway, consisting of core protein kinases Raf, MEK and effector kinases ERK1/2, regulates various biological outcomes such as cell proliferation, differentiation, apoptosis, or cell migration. Signal transduction through the ERK signaling pathway is tightly controlled at all levels of the pathway. However, it is not well understood whether ERK pathway signaling can be modulated by the abundance of ERK pathway core kinases. In this study, we investigated the effects of low-lev ...[more]

PMID: 35933033

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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

RNA-seq of canine MDCK epithelial cell line compared to cell line overexpressing ERK2 or cell line with conditional activation of the ERK pathway

Publications

ERK2 signaling regulates cell-cell adhesion of epithelial cells and enhances growth factor-induced cell scattering.

Similar Datasets

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