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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from control siRNA and M-NM-2-catenin siRNA transfected cultured mouse dermal cells

ABSTRACT: M-NM-2-catenin activity of dermal cells is crucial for hair follicle neogenesis and strongly suggest that transcriptional target genes of M-NM-2-catenin pathway are essential for maintaining trichogenicity of dermal cells. We used microarrays to identify genes targeted by the M-NM-2-catenin pathway that are essential for maintaining the trichogenicity of dermal cells. Freshly isolated dermal cells from the dorsal skins of C57BL/6 neonates (P0) were cultured for 24 hours and transfected with either control siRNA or M-NM-2-catenin specific siRNAs (M-NM-2-catenin siRNA) at a final concentration of 10 nM for 48 hours followed by RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: seung hyun shin

PROVIDER: E-GEOD-50525 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from control siRNA and β-catenin siRNA transfected cultured mouse dermal cells

Project description:β-catenin activity of dermal cells is crucial for hair follicle neogenesis and strongly suggest that transcriptional target genes of β-catenin pathway are essential for maintaining trichogenicity of dermal cells. We used microarrays to identify genes targeted by the β-catenin pathway that are essential for maintaining the trichogenicity of dermal cells.

2013-09-03 | GSE50525 | GEO

Transcriptional profiling of SmoM2 expressing IFE cells at different stages of basal cell carcinoma formation

Project description:Basal cell carcinoma initiating cells undergo profound and rapid reprogramming into embryonic hair follicle progenitor like fate upon SmoM2 expression. Activation of Wnt/M-NM-2-catenin signaling pathways is required in a cell autonomous manner for the reprogramming of adult IFE progenitors into EHFP-like fate as well as for tumor initiation. We used MA to define the molecular changes that occur in basal cell carcinoma initiating cells form the first oncogenic hit to the development of invasive tumor and further on to investigate the role of Wnt/M-NM-2-catenin signaling activation in molecular changes occurring early during BCC development. Basal interfollicular cells expressing SmoM2 were FACS isolated at different stages of tumor development and in M-NM-2-catenin LOF condition for RNA extraction and hybridization on Affymetrix microarrays. By comparing the transcriptional profile of SmoM2 expressing cells with FACS-isolated cells from littermate control mice, we determined a list of genes differentially regulated by SmoM2 expression as specific SmoM2 signature.

2012-09-06 | E-GEOD-40612 | biostudies-arrayexpress

Deciphering the Wnt-dependent gene signature in colorectal cancer cells

Project description:Microarray-based gene expression data were generated from RNA from Ls174T colorectal carcinoma cell lines in which Wnt-dependent transcriptional activity can be abrogated by inducible overexpression of a dominant-negative form of Tcf4 or siRNA against M-NM-2-catenin. shRNA against M-NM-2-catenin, or a dominant-negative Tcf4 transgene, were induced in Ls174T cells for 72 or 24 hours, respectively. Uninduced cells were used as a control. Three replicates per condition.

2011-11-29 | E-GEOD-18560 | biostudies-arrayexpress

Beta-catenin target genes in colorectal carcinoma cell lines with deregulated Wnt/beta-catenin signaling

Project description:To validate the suitability of two commonly used colorectal cancer cell lines, DLD1 and SW480, as model systems to study colorectal carcinogenesis, we treated these cell lines with beta-catenin siRNA and identified beta-catenin target genes using DNA microarrays. The list of identified target genes was compared to previously published beta-catenin target genes found in the PubMed and the GEO databases. Based on the large number of beta-catenin target genes found to be similarly regulated in DLD1, SW480 and LS174T as well as the large overlap with confirmed β-catenin target genes, we conclude that DLD1 and SW480 colon carcinoma cell lines are suitable model systems to study beta-catenin regulated genes and signaling pathways 12 arrays (2 cell lines, 2 treatments, 3 biological replicates)

2013-12-31 | E-GEOD-44097 | biostudies-arrayexpress

Redifferentiation of adult human M-NM-2 cells expanded in vitro by inhibition of the WNT pathway

Project description:In vitro expansion of adult human islet M-NM-2 cells is an attractive solution for the shortage of tissue for cell replacement therapy of type 1 diabetes. Using a lineage tracing approach, we have demonstrated that M-NM-2-cell-derived (BCD) cells rapidly dedifferentiate in culture and can proliferate for up to 16 population doublings. Dedifferentiation is associated with changes resembling epithelial-mesenchymal transition (EMT). The WNT pathway has been shown to induce EMT and plays key roles in regulating replication and differentiation in many cell types. Here we show that BCD cell dedifferentiation is associated with M-NM-2-catenin translocation into the nucleus and activation of the WNT pathway. Inhibition of M-NM-2-catenin expression in expanded BCD cells using short hairpin RNA resulted in growth arrest, mesenchymal-epithelial transition, and redifferentiation, as judged by activation of M-NM-2-cell gene expression. Furthermore, inhibition of M-NM-2-catenin expression synergized with redifferentiation induced by a combination of soluble factors, as judged by an increase in the number of C-peptide-positive cells. Simultaneous inhibition of the WNT and NOTCH pathways also resulted in a synergistic effect on redifferentiation. These findings, which were reproducible in cells derived from multiple human donors, suggest that inhibition of the WNT pathway may contribute to a therapeutically applicable way for generation of functional insulin-producing cells following ex-vivo expansion. Gene expression was studied for beta-cells (4 donors). Dedifferentiation was induced by inhibition of M-NM-2-catenin expression using shRNA. The experiment was performed in 4 batches (see the 'Date' characteristic in the Sample records).

2014-08-27 | E-GEOD-60803 | biostudies-arrayexpress

Gene expression analysis in mouse embryonic stem cells containing Î²-catenin lysine 49 to alanine mutation

Project description:Î²-Catenin is the major co-regulator of the Wnt signalling pathway. Î²-Catenin lysine 49 is post-translationally modified. The histone methyl transferase Ezh2 trimethylates Î²-catenin at lysine 49 and the acetyl transferase Cbp acetylates Î²-catenin at the same lysine. To determine the effects on gene expression embryonic stem cells containing either a Gfp tagged Î²-catenin wildtype (wt) or lysine 49 to alanine (K49A) loss of function mutation were analysed by micro array expression profiling. To determine the effects on gene expression in the pluripotent state two biological replicates of Gfp Î²-catenin wt and Gfp Î²-catenin K49A were analysed. The results showed that genes which affect pluripotency as well as differentiation were altered by Î²-catenin K49A mutation. To analyse the effects of gene expression during ES cell differentiation ES cells containing Gfp Î²-catenin wt or K49A were differentiated into mesodermal progenitors (mp) and neuronal progenitors (np). Two biological replicates were analysed by micro array expression profiling. Differentially expressed genes between Gfp Î²-catenin wt and K49A during differentiation were observed. Mesodermal marker genes like t-brachyury and cdx2 were not upregulated in mesodermal differentiation of Gfp Î²-catenin K49A Es cells.

2017-03-21 | E-MTAB-5523 | biostudies-arrayexpress

Characterisation of the Beta-Catenin cytoplasmic/nuclear interactome in leukaemia cells

Project description:Canonical Wnt/B-catenin signaling is frequently dysregulated in myeloid leukemias and is implicated in leukemogenesis. Nuclear-localized β-catenin is indicative of active Wnt signaling and is frequently observed in acute myeloid leukemia (AML) patients; however, some patients exhibit little or no β-catenin nuclear-localization even where cytosolic B-catenin is abundant. Differential propensity for nuclear-localized β-catenin is also observed in cell lines. To investigate the factors mediating the nuclear-localization of B-catenin we carried out a nuclear/cytoplasmic proteomic analysis of the B-catenin interactome in myeloid leukemia cells. From this we identified hundreds of putative novel B-catenin-interactors. Comparison of interacting factors between Wnt-responsive cells (high nuclear B-catenin, K562/HEL) versus Wnt-unresponsive cells (low nuclear B-catenin, ML1) suggested the established interactor, LEF1, is a key factor mediating the nuclear-localization of B-catenin in myeloid leukemia. The relative levels of nuclear LEF1 and B-catenin were tightly correlated in both cell lines and in primary AML blasts. Furthermore, LEF1 knockdown inhibited B-catenin nuclear-localization and transcriptional activation in Wnt-responsive cells. Conversely, LEF1 overexpression was able to promote both nuclear-localization and B-catenin-dependent transcriptional responses in previously Wnt-unresponsive cells. This study is the first to present a B-catenin interactome in hematopoietic cells and reveals LEF1 as a critical regulator of canonical Wnt signaling in myeloid leukemia.

2019-01-11 | PXD009305 | Pride

Gene expression profiling of C/EBPM-NM-2- and STAT3-deficient human endometrial stromal cells (HESC)

Project description:Our previous studies have shown that C/EBPM-NM-2 plays a critical role in human endometrial stromal decidualization. In order to identify the molecular pathways regulated by C/EBPM-NM-2 during decidualization, we performed gene expression profiling using RNA isolated from normal and C/EBPM-NM-2-deficient human endometrial stromal cells. The microarray results revealed that several key regulators of stromal differentiation, such as BMP2, Wnt4, IL-11RM-NM-1 and STAT3, operate downstream of C/EBPM-NM-2 during decidualization. Further studies revealed that STAT3 is a direct target of C/EBPM-NM-2 and plays an important role in cytokine signal during the decidualization process. Gene expression profiling, using STAT3-deficient HESCs, showed an extensive overlap of pathways downstream of STAT3 and C/EBPM-NM-2 during stromal cell differentiation. We employed a siRNA strategy to suppress C/EBPM-NM-2 or STAT3 mRNA expression in HESCs and then performed microarray analysis to identify its downstream target genes. Further, using a similar strategy, we focused on STAT3, a C/EBPM-NM-2 target gene, and identified the commone pathways downstream of both C/EBPM-NM-2 and STAT3.

2012-10-11 | E-GEOD-41473 | biostudies-arrayexpress

Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor M-NM-11 apoprotein

Project description:Under conditions of hormonal adjuvant treatment the estrogen receptor apoprotein supports breast cancer cell cycling through the retinoic acid receptor M-NM-11 apoprotein. Basal proliferation persisted in estrogen-sensitive breast cancer cells grown in hormone depleted conditioned media without or with 4-hydroxytamoxifen (OH-Tam). Downregulating ER using siRNA inhibited basal proliferation by promoting cell cycle arrest. The basal expression of RARM-NM-11, the only RARM-NM-1 isoform that was expressed in breast cancer cell lines and in most breast tumors, was supported by apo-ER but was unaffected by OH-Tam. The overlapping tamoxifen-insensitive gene regulation by apo-ER and apo-RARM-NM-11 comprised activation of mainly genes promoting cell cycle and mitosis and suppression of genes involved in growth inhibition. Cells were plated at 20% confluence in low glucose phenol red free medium supplemented with 5% charcoal stripped FBS and glutamine 24h-48h prior to transfection. Treatment with vehicle, OH-Tam (100nM), or OH-Tam (500nM) was begun an additional 24h later. Cells were transfected with control siRNA, ERM-NM-1 siRNA or RARM-NM-1 siRNA.

2011-05-13 | E-GEOD-26298 | biostudies-arrayexpress

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Project description:Mouse primary dermal fibroblasts were treated with 100 nM endothelin-1 (ET1) synthetic peptide for 24 hours. Control samples received no ET1 peptide. The experiment compared treated to untreated to identify gene expression changes due to ET1 exposure. There are three biological replicates for both control and treated samples. These biological replicates represent separate derivations of primary dermal fibroblasts from genetically identical mouse litters aged 0-3 days.

2005-01-01 | E-MEXP-700 | biostudies-arrayexpress

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